The authors [19] concluded that germline monoallelic inactivation of MUTYH is not sufficient for C:G>A:T transversion somatic signatures previously correlated with MUTYH deficiency to arise but that biallelic complete loss of function of the MUTYH gene is necessary to cause tumors similar to those associated with polyposis due to biallelic mutations in the MUTYH gene. The gene discussed is MUTYH; the disease is polyposis.