Radiation-induced premature aging of BM HSCs is characterized by elevated levels of aging markers (such as SA-β-gal, p16, and Arf), impaired self-renewal capacity, diminished long-term reconstruction ability, and increased myeloid-biased differentiation, accompanied by a decline in overall immune and anti-infection capabilities [2, 10, 11]. The gene discussed is CDKN2A; the disease is infection.