To investigate whether blocking the PI3K/AKT signaling can largely abolish the promoting effect of GLS2 knockdown on the anchorage-independent growth of HCC cells and the growth of HCC xenograft tumors, the DN-AKT (K179M) was stably expressed in PLC/PRF/5 cells with stable GLS2 knockdown (Figure 5D). This evidence concerns the gene AKT1 and hepatocellular carcinoma.