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). This evidence concerns the gene MCL1 and colorectal carcinoma.