As for MED12, it was altered in 10% of our T-ALL patients and was as frequently mutated as the known T-ALL gene NRAS. The loss-of-function mutations in MED12 (p.V167fs and splice site g.chrX:70339329T>C) were both shown to be expressed, supporting a functional role of these mutations in T-ALL. Here, MED12 is linked to acute lymphoblastic leukemia.