Semaphorins are an important class of chemorepellents and have been linked to guidance of interneurons. Marin et al. have reported that the effect of semaphorins (3A/3F) is modulated by whether or not the interneurons express neuropilin: those cells that do are guided to the cortex, whereas the rest terminate in the striatum\cite{Marin_2001}.  One study showed that Sema3a in conjunction with chondroitin sulfate keep interneurons from entering the striatal mantle zone \cite{Zimmer_2010}
 Ephrin-A5 signalling from the ventricular zone repulses interneurons from the mGE and may therefore provide the initial impetus for interneurons to leave the mGE \cite{Zimmer_2008}. Interneurons migrating from the mGE express the EphA4 receptor, which is repelled by ephrin-A3 signalling from the developing striatum \cite{Rudolph_2010}. Similarly, interneurons originating from the POA express EphB1/3 and are repulsed by the ephrin-B3 expressed in the POA because the activation of the EphB1 receptor induces the phosphorylation of Src and Fak, which creates a cascade the results in repulsion \cite{Rudolph_2014}.  A recent study has found that ephrin-B acts as receptor for EphB on radial glial cells to promote reverse signalling  \cite{Talebian_2017}. Meanwhile EphB on the interneuron acts as a receptor for ephrin-B2 bound to radial glial cells and  promotes forward signalling \cite{Talebian_2017}. A balance of both forward and reverse signalling, via Eph-B receptors and transmembrane ephrin proteins, seems to be essential for establishing the proper interneuron distribution. 
There is in vitro evidence that Slit and its receptor, Robo, form a chemorepulsive signalling mechanism for interneuron migration \cite{Zhu_1999}, but the actual role this plays for interneuron migration in vivo is not clear.  Only rodents with mutations in Robo, but not Slit, show an abnormal distribution in the number of interneurons neurons \cite{Marin_2003,Andrews_2008} .  Nonetheless, because Slit-deficient rodents exhibit defects in the type of interneurons distributed in the cortex, is appears that Slit may play an important role for guiding cells once they have arrived at the cortex \cite{Marin_2003}. For example, Wichterle et al. found that the mGE is surrounded by inhibitory signalling, mostly from Slit1 and Slit2, and that a permissive dorsal migratory is formed by chemoattractants \cite{Wichterle_2003}.
4. Chemoattractants 
In addition to being pushed by chemorepellants, several signalling pathways have been implicated in attracting interneurons to the cortex. Neuregulin 1 (Nrg1) is a cell adhesion molecule that is expressed in a membrane-bound form in the  lGE and an unbound isoform of Nrg1 in the cortex. It has an epidermal growth-factor domain that binds to the ErB4 in interneurons, the loss of which leads to an abnormal corical interneuron distribution \cite{Flames_2005}. As previously mentioned, ephrin can also act as a chemoattractant via reverse signalling mediated by ephrin A and B ligands \cite{Steinecke_2013}.
Chemoattractants not only bring interneurons to the cortex, but also help to determine where in the cortex the interneurons will go. CXCL12 via an interaction with CXCR4 acts as a chemoattractant for interneurons whose role is not so much to guide interneurons to the cortex, but rather to make sure they end up in the appropriate location and cortical layer \cite{Daniel_2005,Tiveron_2006,Stumm2003}.  Interneurons will normally avoid entering the cortical plate for approximately 48 hours after reaching the cortex, during which time they spread out tangentially  \cite{López-Bendito2008}. However, distrubing the usual CXCL12 and CXCR4 signalling leads to early entry of the interneurons into the cortex and thus abnormal interneuron distribution \cite{López-Bendito2008}. CXCL12-CXCR4 are also important for getting interneurons to enter the migratory streams they will follow to the cortex \cite{Li2008}.
5. Neurotransmitters
Neurotransmitters also appear to play a role in migration, especially GABA and dopamine. Migrating internruons express increaresed sensitivity to GABA through an upregulation of GABAA and GABAB receptors \cite{Cuzon_2005,Cuzon_Carlson_2010}. Reducing GABA levels in the cortex leads to a decrease in the number of interneurons that cross into the cortical wall  \cite{Cuzon_2005,Lopez_Bendito_2003}. In addition, migrating interneurons also have D1 and D2 dopamine receptors\cite{Crandall_2007,Ohtani2003}. Whereas D1 nulls show decreased ability to migrate, D2 knockoutss are show an increased propensity to migration\cite{Crandall2007}. This suggests that D1 and D2 normally function to promote or inhibit, respectively, cortical interneuron migration. Finally, neurotransmitters may play a role in halting interneuron migration. One study has found that an upregulation of the KCC2 potasium-chloride pump leads to a hyperpolarization of the neurons when GABAR channels are opened and thus signals and end to cell motility \cite{Bortone_2009}
6. Discussion 
Why are there two mechanisms of migration? Radial migration produces a one to one mapping between the originating location in the embryonic brain and the final destination in the cortex. Tangential migration does not depend on physical pathways established by RGCs and thus allows neurons from a given region to be distributed to multiple cortical regions in a one-to-many pattern. This may allow for an increase in the complexity of the cortical circuitry.