Interestingly, in the AOM-DSS- and the DSS-induced colitis models, the rate of tumor development after recovery from colitis is increased in Fn14-deficient mice but also in TNFR1-deficient mice possibly reflecting insufficient TNFR1/Fn14-mediated IEC apoptosis leading to uncontrolled compensatory proliferation and/or outgrowth of yet less apoptosis-sensitive precancerous cells eventually resulting in cancer development (Popivanova et al., 2008; Di Martino et al., 2016). This evidence concerns the gene TNFRSF12A and neoplasm.