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). The gene discussed is RAB2A; the disease is Hepatic steatosis.