Over 40% of t(12;21) leukemias carry deletions in genes affecting B‐lineage maturation as well as G1/S cell cycle progression checkpoint genes such as CDKN2A,51 while in t(8;21) leukemias drivers of proliferation predominate, with more than 50% of tumors harboring KIT, NRAS, KRAS, FLT3‐ITD, TKD, CBL, or JAK2 mutations.52 Finally, as leukemia and lymphoma cells display resistance to RUNX SLGA, and may even become addicted to RUNX,13, 21, 53 it is possible that drugs directly targeting RUNX‐CBFB functions may have a role to play in future therapeutic strategies.54 The gene discussed is NRAS; the disease is lymphoma.