BCL2 and colorectal carcinoma: Moreover, we identified that the aberrantly active WNT/β-catenin signaling in CRC cells was suppressed upon DHME stimulation (Figure 4), and notably, the ectopic expression of a dominant–active β-catenin mutant (∆N90-β-catenin) abolished DHME-induced CRC cytotoxicity, likely due to sustained BCL-2 expression in the context of constitutive β-catenin activation (Figure 5).