In fact, it has been observed that small molecule-mediated activation of CK1α decreases proliferation[25] whereas targeted deletion of CK1α, when combined with p53 or p21 deletion, enhances proliferation resulting in small bowel carcinoma.[26] It is possible that the D163N mutation characterized in patient 815zp led to enzymatic inactivation of CSNK1A1 and ultimately promoted, perhaps when combined with other mutation(s), the development of colon cancer. This evidence concerns the gene TP53 and small intestine carcinoma.