Analyses integrated with tumor-intrinsic and immune cell-focused features showed that nuanced characteristics of the tumor genomic landscape together with proinflammatory signatures in TME could better distinguish responding from non-responding tumors (9, 50, 51)—for instance, the recruitment of TAMs to tumors is mainly mediated by a range of tumor-derived chemokines, including CCL2, VEGF, CCL5, and CSF1 (41). The gene discussed is CCL5; the disease is neoplasm.