Contrary to the tumor microenvironment, in other inflammatory conditions, such as in transplantation settings or autoimmunity, Tregs lose their suppressive function and convert into effector cells that produce pro-inflammatory cytokines (IFNγ, IL-17, IL-4) and have increased expression of associated master regulator transcription factors (such as T-bet, IRF4, and RORγt, or IRF4 and GATA3). This functional impairment of Tregs causes loss in FOXP3 expression as well as hyperactivation of the inflammatory PI3K pathway [77].