NF-κB was previously showed as a barrier for reprogramming, and DOT1L served as a prominent effector of NF-κB signaling.8 Moreover, NF-κB pathway was highly activated in human T-ALL and inhibition of the pathway could significantly restrict the development of Notch1-induced T-ALL.13 suggesting that the oncogenesis of T-ALL was apparently different from the induced pluripotent reprogramming progress. The gene discussed is DOT1L; the disease is acute lymphoblastic leukemia.