RAB2A and metabolic dysfunction-associated steatotic liver disease: It was shown that TBC1D1S231A-knock-in (KI) mice inhibit the phosphorylation of AMPK-TBC1D1 signaling through nutritional supplementation, block the AMPK-TBC1D1 pathway, increase the level of GTP-bound Rab2A, which in turn improves the protein stability of PPARγ and ultimately promotes the accumulation of intra- and extrahepatic lipids and leads to NAFLD in aged mice [48].