Besides, we found that dysregulated proliferation of IECs in non-dysplastic and dysplastic areas of the colon in the absence of RIPK3 was accompanied with heightened activation and phosphorylation of AKT, further confirming the mechanism that RIPK3 protects against colitis-associated CRC by repressing excessive IEC proliferation. The gene discussed is AKT1; the disease is colorectal carcinoma.