ALKBH5 and neoplasm: Genetic deletion or pharmacological inhibition of ALKBH5 (e.g., IOX1) significantly enhanced the efficacy of anti–PD-1 therapy, resulting in tumor regression, increased infiltration of cytotoxic lymphocytes, and elevated proinflammatory cytokines, supporting the preclinical feasibility of ALKBH5 inhibition combined with ICIs (62).