In this study, we unraveled BCL-2 as a possible downstream effector of WNT/β-catenin signaling to promote CRC cell survival, as evidenced by the resistance of BCL-2 to DHME-mediated downregulation, along with DHME-induced apoptosis when β-catenin was constitutively active (Figure 5). Here, BCL2 is linked to colorectal carcinoma.