Our data thus suggest that KMT2C may be important for regulation of estrogen signaling in CRC tumorigenesis, but unlike previous reports in breast cancer [49], we saw minor effects of PRSS23 knockdown on CRC cell proliferation, suggesting the possibility that other KMT2C regulated genes are more important for promotion of CRC tumorigenesis following loss of KMT2C. Here, KMT2C is linked to breast carcinoma.