A Nature Communications paper from Zhang, Ma, Wan and colleagues identifies histone lactylation as an epigenetic driver of immune evasion in pancreatic ductal adenocarcinoma. The work shows lactylation upregulates CXCL1 expression, reshaping the tumor microenvironment to suppress antitumor immunity and blunt checkpoint responses. Authors mapped the lactate‑to‑histone modification axis, combined molecular perturbation with immune profiling and demonstrated that targeting lactylation or downstream CXCL1 signaling restored immune activity in preclinical models. The findings reveal a metabolic‑epigenetic mechanism that could be targeted to sensitize immunologically cold pancreatic tumors to immunotherapy.