The development of neuroendocrine differentiation is considered to be a later event, as neuroendocrine components of CRCs share the common mutations of the non‐neuroendocrine parts, including mutations in APC, TP53, and KRAS. 68, 69It has been suggested that the development of neuroendocrine cells in adenomas or adenocarcinomas is influenced by the phosphoinositide 3‐kinase–Akt–mammalian target of rapamycin pathway.70 This evidence concerns the gene MTOR and adenocarcinoma.