Mutations and rearrangements in several genes have been implicated in T-ALL, such as in HOX genes, genes regulating RAS signaling (e.g. FLT3), histone-modifying genes (e.g. EZH2), transcription-factor tumor suppressors (e.g. AML1, ETV5 or LEF1), mutations affecting the NOTCH1 pathway, and many more. The gene discussed is RUNX1; the disease is acute lymphoblastic leukemia.