It is well-established that the pro-survival PI3K-Akt-mTOR axis is abnormally upregulated in AML patients, through various molecular mutations (e.g., receptor tyrosine kinases, GTPases, FLT3-ITD) (Kandoth et al., 2013; Weinstein et al., 2013), with constitutive induction of this pathway occurring on average in almost two thirds of AML patients, and correlating with inferior survival (Min et al., 2003; Xu et al., 2003; Kornblau et al., 2009; Chen et al., 2010; Nepstad et al., 2019, 2020). The gene discussed is FLT3; the disease is acute myeloid leukemia.