Although gankirin-mediated resistance to sorafenib was completely blocked by the knockdown of ATG7, CQ, or 3-MA in HCC cells, indicating that autophagy is a mechanism associated with sorafenib resistance (discussed on Section 4), sorafenib induced an increase in LC3 lipidation and p62 degradation triggered by AKT inhibition in a MAPK-independent autophagy-mediated cell death in ACHN and 786-O renal carcinoma cell lines. The gene discussed is AKT1; the disease is hepatocellular carcinoma.