As a result, there was enhanced apoptosis in these cells.18 Convincingly, they showed that treatment with antioxidant N-acetyl cysteine in those Bmi1-downregulated AML cells led to decreased reactive oxygen species accumulation and restored progenitor frequencies, which further confirmed the Bmi1-conferred protective effects of leukemic blasts against apoptosis. The gene discussed is BMI1; the disease is acute myeloid leukemia.