In a study meticulously delineating the intricate structure and mechanism of DNMT3A protein’s, it was illuminated that the DNMT3A-DNA interplay—encompassing a target recognition domain, a catalytic loop, and a DNMT3A homodimeric interface—revealed that somatic mutations associated with hematological cancers within the substrate-binding residues not only attenuate DNMT3A activity but also precipitate CpG hypomethylation, thereby catalyzing the transformation of hematopoietic cells (78). The gene discussed is DNMT3A; the disease is hematopoietic and lymphoid cell neoplasm.