To understand the molecular mechanisms underlying AML transformation upon combined mutation in TET2 and TP53, we performed bulk RNA-Seq of Lin–cKIT+ myeloid progenitors (LK) and Lin–cKIT+Sca-1+ (LSK) cells from diseased Vav-cre Tet2fl/flTp53fl/fl mice developing AML and age-matched Vav-cre Tp53fl/fl, Vav-cre Tet2fl/fl, and WT mice. The gene discussed is TP53; the disease is acute myeloid leukemia.