DNMT3A mutation leads to high expression of nicotinamide adenine dinucleotide (NAD) salvage synthesis pathway key enzyme, nicotinamide-phosphate ribosyltransferase (NAMPT), through DNA hypomethylation, which ultimately leads to abnormal nicotinamide (NAM) metabolism and NAD synthesis, which provides a potential direction for targeting DNMT3A-mutated acute myeloid leukaemia from metabolic level [141]. This evidence concerns the gene DNMT3A and acute myeloid leukemia.