BCL2 and colorectal carcinoma: In addition to the suppression of ERK signaling, other mechanisms have been reported to mediate the proapoptotic effect of ER calcium release, such as activation of calcium/calmodulin‐dependent protein kinase II[32] or disruption of mitochondrial structure/function by interfering with antiapoptotic molecules BCL‐2, BCL‐xL, and MCL1, resulting in cytochrome c release after fluxing into the mitochondria.[27b] In addition to the ER calcium release, we also identified the specific activation of the PERK‐eIF2a‐ATF4‐CHOPER stress pathway in CRC cells treated with NK‐1R antagonists (Figure 4E).