While KAT2A has been implicated in tumorigenic processes,34,37 our work provides direct evidence of its HCC-specific role: KAT2A ablation suppressed malignant progression in preclinical models predominantly mediated through SRSF11 succinylation attenuation and established a causal hierarchy wherein KAT2A-mediated succinylation licenses the oncogenic functionality of SRSF11. The gene discussed is KAT2A; the disease is hepatocellular carcinoma.