Although DNMT3A mutations are frequent in acute myeloid leukemia, myeloproliferative disorders, and T-ALL [221], it is not an expected lesion within CLL; instead, several works demonstrated that low activity and expression of DNMT3A is important for CLL pathogenesis and evolution [222,223,224], and mouse models with deletion of Dnmt3a consistently developed CLL [225]. Here, DNMT3A is linked to acute lymphoblastic leukemia.