As expected, compared with corresponding control groups, activated AMPK not only increased ENO2 expression levels of co-cultured resistant HCC cells, (Fig. 6L, M; Supplemental Fig. S7I) but also attenuated the inhibitory effects of CCHuh7R-shENO2 on the above glycolysis indicators (excepting unchanged AMPK protein expression level) and cell competition phenomenon (Supplemental Fig. S7J–M), suggesting that AMPK-regulated glycolysis and competitive dominance of CCHuh7R/CCPLC-PRF-5R required the existence of ENO2. This evidence concerns the gene PRKAA2 and hepatocellular carcinoma.