In the present study, by using a murine model of CRMAC, in which C57 wild type and loss-of-function c-kit mutant Wads−/− type mice were treated with AOM+DSS for longer time than usual, we showed that the c-kit signaling evidently promoted tumor growth by decreasing p53 and increasing cyclin D1. This evidence concerns the gene CCND1 and neoplasm.