Haploinsufficiency of the c-myc transcriptional repressor FIR and the FIR+/−TP53−/− genotype in mice potently promoted the progression of T-ALL/lymphoma, at least in part by activating the Notch signaling pathway with c-myc/c-Myc upergulation. The gene discussed is MYC; the disease is acute lymphoblastic leukemia.