LKB1 stabilizes FOXP3 expression in Tregs that maintain immunological self-tolerance and homeostasis [80]. Di Wu et al. have reported that LKB1 governs Treg survival and its lineage identity [80]. T cell's specific deletion of LKB1 causes a halt in Treg regulatory function that leads to impaired immune responses [80, 87]. Moreover, LKB1 deficient Tregs have been characterized by defective mitochondria, compromised OXPHOS, depleted cellular ATP, and altered cellular metabolism pathways [80]. Treg-specific deletion of LKB1 leads to the development of fatal autoimmune inflammation [80, 88], and causes disrupted Treg survival and reduced mitochondrial mass, its membrane potential, and increased the generation of ROS [85, 86, 89]. Mechanistically, LKB1 deficiency causes the diminished release of intracellular ATP and induces aberrant expression of immune regulatory molecules such as PD-1, and TNF receptor GITR, and OX40 [85, 90-93]. Yang K et al. in his classic work has been reported that LKB1 function in Tregs does not depend on AMPK signaling or the mTORC1–HIF-1α axis as described earlier, however, it depends on LKB1-β-catenin signaling to regulate PD-1 and TNF receptor proteins such as GITR and OX40 expression on Treg cell  [9, 21, 85]. β-catenin is a key mediator of Wnt signaling and suppresses the aberrant expression of PD-1 and GITR in Treg cells. LKB1 deficient Treg cells show the degradation of β-catenin. Briefly, these findings indicate the role of LKB1-β-catenin signaling in the control of Th2 response by modulating PD1 and other Treg signature molecules [85, 94].