Given that TP53 mutations or loss are frequently detected in patients with therapy-related AML or AML with complex karyotype,27, 28 we therefore next explored whether MEG3 plays a role as tumor suppressor in AML cell lines absent of TP53. As in the TP53wt AML cell line, stable overexpression of MEG3 in the two TP53mut AML cell lines U937 (WT1mut, TET2wt) and HL-60 (WT1wt, TET2wt) significantly suppressed cell proliferation, induced G0/G1 cell cycle arrest and apoptosis when compared to controls (Figures 2h–k). The gene discussed is TP53; the disease is neoplasm.