Our findings also highlighted a novel FATP5-mediated AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) signaling pathway in HCC cells that regulates the invasive and EMT phenotype by reprogramming intracellular glycolysis and energy metabolism, thus providing potential therapeutic targets to develop treatment strategies for FATP5-dependent HCC. The gene discussed is PRKAA1; the disease is hepatocellular carcinoma.