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. The gene discussed is PIM1; the disease is acute lymphoblastic leukemia.