Our group and others previously identified constitutive JAK/STAT, PI3K/mTOR, and BCR-like/SFK signaling in primary Ph-like ALL cells and associated patient-derived xenograft (PDX) models, providing rationale for development of tyrosine kinase inhibitor (TKI)-based therapies that may improve clinical outcomes for patients with these chemoresistant leukemias [10–14]. This evidence concerns the gene SOAT1 and leukemia.