In high-grade serous ovarian carcinoma, tumor cells reprogram fibroblasts through TGF-β and inflammatory signaling, generating distinct CAF states that reciprocally promote tumor growth, ECM remodeling, and immune suppression via IL-6/signal transducer and activator of transcription 3 (STAT3) and CXCL12 signaling [22,25,26,27]. The gene discussed is CXCL12; the disease is neoplasm.