The identification of specific genetic lesions is important for guiding targeted therapeutic intervention as a proportion of kinase-activating alterations in Ph-like ALL can, at least based on in vitro and preclinical models, be targeted by FDA-approved TKIs: JAK-STAT signaling (JAK inhibition); ABL-class fusions (ABL inhibitor); FLT3 and NTRK3 fusions (FLT3 and NTRK3 inhibitor) [104]. This evidence concerns the gene SOAT1 and acute lymphoblastic leukemia.