TET1 plays an indispensable role in hematopoiesis by regulating target genes that mediate leukemic transformation [39] and is considered to be a tumor suppressor (mutated in 14% of T‐ALL patients,see Table 1) [40] except in MLL‐rearranged leukemias, where it acts as an oncogene, facilitating leukemogenesis by being directly activated by MLL fusion proteins and upregulating the expression of key oncogenic target genes such as HOXA9, MEIS1, and PBX3 [39]. The gene discussed is KMT2A; the disease is neoplasm.