According to the mechanism, Figure 6A shows that antrodin C treatment induced both death-receptor-mediated extrinsic apoptosis (caspase-3, caspase-9, Bax, and TNFα) and the mitochondria-mediated apoptotic pathway (Bcl-2) in CRC, followed by altering the assembly of decreased cell-cycle-related proteins such as cyclin D1 and cyclin E [46]. Here, BAX is linked to colorectal carcinoma.