To validate these findings in a well‐defined genetic setting marked by APC loss, we took advantage of murine tumor organoids (MTOs) established from murine intestinal tumors bearing deletions or mutations in the four key human CRC driver genes Apc, Kras, Tgfbr2, and Trp53 [22]. The gene discussed is TGFBR2; the disease is intestinal neoplasm.