Recently, Wu et al. reported that in FLT3-ITD-mutated AML, FLT3-ITD signaling can upregulate the expression of key DNA damage response (DDR) factors, e.g, Wee1-like protein kinase (WEE1), checkpoint kinase 1 (CHK1), proviral integration site for Moloney murine leukemia virus-1 (PIM-1), radiation sensitive 51 (RAD51), and mismatch repair (MMR) factors, e.g, MutS homolog 2 (MSH2), MSH6 and MutL homolog 1 (MLH1) through the STAT5 and ERK pathways, respectively (Fig. 2). The gene discussed is PIM1; the disease is acute myeloid leukemia.