CDK9i monotreatment enhances the proportions of CD45+ immune cells and CD3+ T cells, activates dendritic cells, and synergistically augments immune responses when combined with checkpoint blockade.[16] Our study further elucidated that CDK9i activated the complement system, specifically the C1r/C3a/C3aR axis, which emerges as an important component of tumor‐promoting inflammation, characterized by increased accumulation of educated TAMs and neutrophils. The gene discussed is C1R; the disease is neoplasm.