In this context, monoallelic MUTYH variants are frequently identified in patients with early‐onset or familial cancers, and some tumors from these individuals display molecular features similar to those of biallelic cases (e.g., G:C>T:A transversions and signature 36), suggesting a potential pathogenic role, especially in the presence of somatic loss of heterozygosity [17]. This evidence concerns the gene MUTYH and cancer.