Importantly, studies in bone marrow chimeras established that hematopoietic cells are the main driver of CA-CRC development in Irf1−/− mutants, as Irf1−/− BM can transfer CA-CRC susceptibility to control B6, while B6 BM can protect Irf1−/− mutants against CA-CRC. This evidence concerns the gene IRF1 and colorectal carcinoma.