[4, 45, 46] Our data demonstrated, for at least Flt3ITD+ve/TET2mut/hypomorphic AML, a more complex and cooperative remission-inducing mitigation, by epigenetic combinations causing de-repression/upregulation of Wnt antagonist RUNX3, and affecting severe ID1 and JUN/c-jun depletion, which were associated with HOXA depletion.[6, 9, 12, 20] By contrast, mechanistic linkage to CDKN2A/DAPK1 de-repression was infrequent. The gene discussed is JUN; the disease is acute myeloid leukemia.