Our results are consistent with a composite model in which overnutrition attenuates the phosphorylation levels of AMPK-TBC1D1 signaling and augments the GTP-bound active Rab2A, which consequently promotes hepatic steatosis through increasing the protein stability of PPARγ and the expression of PPARγ target genes (Fig 7G). This evidence concerns the gene RAB2A and fatty liver disease.