Of these, RUNX1 variants in B-ALL consistently showed minimal damaging effects, whereas six T-ALL-related variants (p.K117*, p.A142fs, p.S213fs, p.R233fs, p.Y287*, and p.G365R) caused a significant reduction in RUNX1 activity as a transcription activator in vitro. The gene discussed is RUNX1; the disease is acute lymphoblastic leukemia.