The haploinsufficiency of DNMT3A could transform FLT3-ITD myeloproliferative neoplasm (MPN) into AML,152 and cooperate with oncogenic KRAS to promote the development of T-ALL.153 The haploinsufficient tumor suppressor effect of DNMT3A was also reported in CLL,154 CD8+ PTCL,155, and AITL.156–159 Third, DNMT3A mutations were closely related to treatment response. This evidence concerns the gene KRAS and myeloproliferative neoplasm.