DNMT3A loss of function mutations appeared to drive colitis-associated colon cancer growth and progression, although the exact mechanism has not yet been elucidated.90ASXL1 mutations were found to promote tumorigenesis in a variety of cancer models through disrupted T-cell development and functionality.91 Finally, wild-type p53 in myeloid cells was found to suppress M2 macrophage polarization and tumor invasiveness in an intestinal cancer model, indicating a potential cancer risk with TP53 loss-of-function mutations in CH.92 The gene discussed is TP53; the disease is colonic neoplasm.