In HCC, it was shown that the molecular mechanisms by which sorafenib induces autophagy could be independent of AMP-activated protein kinase (AMPK) and involve a reduction in MCL-1 levels, which in turns would inactivate signal transducer and activator of transcription 3 factor (STAT3), causing the accumulation of beclin-1 (BECN-1) and other proteins indicating autophagosome formation, such as LC3B-II accumulation, as well as sequestosome 1 (p62) reduction [25,28,41,49,73]. Here, BECN1 is linked to hepatocellular carcinoma.