To provide a proof of concept that pharmacological modulation of SET is a promising strategy for the treatment of KMT2A-R-leukemia, we tested in vitro FTY720 (Fingolimod), a proven inhibitor of the interaction between SET and PP2A [28, 40–43], that had been shown to induce cell death in several solid tumors and leukemia models by various mechanisms [44, 45, 50, 51]. The gene discussed is PTPA; the disease is leukemia.