Next, we studied the subjacent molecular cascades and revealed that JAK/STAT pathway mutations identified in T-ALL lead to the aberrant activation of c-MYC and mTOR pathways and that such activation can be reversed by PIM447 treatment, proposing the activity of PIM proteins as an essential event to maintain S6 and c-MYC phosphorylation in cells with JAK/STAT pathway mutations. This evidence concerns the gene SOAT1 and acute lymphoblastic leukemia.