This late-onset could be explained by the fact that CMMRD, PMS2/MSH6 homozygous pathogenic variants are associated with a later onset phenotype compared to homozygous pathogenic variants in MLH1/MSH2 genes which result in more aggressive hematological malignancies during young childhood and are associated with a worse prognosis [33]. This evidence concerns the gene MLH1 and hematologic disorder.