SOAT1 and acute lymphoblastic leukemia: Physiological activation of the pathway is induced when IL-7 binds to its cognate receptor, which results in the activation of downstream JAK/STAT and phosphatidylinositol 3-kinase (PI3K)/AKT pathways.40 In T-ALL, IL-7 signaling can be activated both due to IL-7 receptor mutations or after IL-7 stimulation that induces GC resistance through the upregulation of MAPK kinase (MEK)/extracellular signal-related kinase (ERK) and PI3K/AKT/mammalian target of rapamycin (mTOR) pathways, which can in turn be reversed by IL-7 and/or MEK/ERK inhibitor treatment.31,32,41