BCL2 and hepatocellular carcinoma: Importantly, we identified the underlying molecular mechanism by which SAF not only downregulates the expression of MARCH1 but also further inhibits the downstream signaling cascades PI3K/AKT/β-catenin and antiapoptotic Mcl-1/Bcl-2 and activates the cleaved caspase-3 and cleaved caspase-7 signaling pathways to repress the development and progression of HCC with respect to growth, apoptosis, cell cycle, migration, and invasion, both in vitro and in vivo.