["Journal of Cellular Physiology, Volume 241, Issue 6, June 2026. ", "This graphical abstract summarizes the major immune‐evasion mechanisms that limit immunotherapy efficacy in ovarian cancer peritoneal metastasis. Peritoneal dissemination is shaped by impaired antigen visibility, coordinated immune‐evasion modules within ascites and multicellular spheroids, checkpoint‐driven T‐cell exhaustion, suppressive tumor‐microenvironment feedback loops, and metabolic‐epigenetic suppression. Key inhibitory pathways include defective MHC‐I antigen presentation, PD‐1/PD‐L1, CTLA‐4, LAG‐3, TIM‐3 and TIGIT signaling, regulatory T cells, M2‐like macrophages, MDSCs/neutrophils, lactate accumulation, adenosine generation through CD39/CD73, IDO1‐mediated kynurenine production, and arginine depletion. The lower panel links these resistance mechanisms to biomarker‐guided therapeutic strategies, including antigen‐presentation restoration, dual checkpoint blockade, myeloid/TME reprogramming, metabolic‐axis inhibition, PARP inhibitor plus immune checkpoint inhibitor combinations, and intraperitoneal, oncolytic, or cellular therapeutic platforms.\n\n\n\n\n\n\nABSTRACT\nOvarian cancer peritoneal metastasis remains a major cause of recurrence and death despite advances in cytoreductive surgery, platinum‐based chemotherapy, PARP inhibition, and immune checkpoint blockade. The limited activity of immunotherapy in this setting reflects layered immune resistance shaped by impaired antigen visibility, redundant inhibitory receptor networks, suppressive myeloid and regulatory circuits, and metabolic‐epigenetic constraints within ascites and multicellular spheroids. These compartment‐specific features distinguish peritoneal disease from anatomically confined tumors and help explain why systemic immune reinvigoration alone rarely produces durable benefit. Here, we synthesize current evidence on the mechanisms that govern immune escape in ovarian cancer peritoneal dissemination, with emphasis on antigen presentation defects, checkpoint‐driven T‐cell exhaustion, anti‐phagocytic signaling, soluble suppressive mediators, and metabolic remodeling of the ascites microenvironment. We further examine how DNA damage response states intersect with innate immune sensing and discuss the translational implications of homologous recombination deficiency for combination treatment design. Finally, we propose a biomarker‐guided framework that links antigen‐presentation competence, immune engagement, dominant suppressive axes, and ascites‐specific biology to rational therapeutic matching. This mechanism‐centered view supports more precise trial design and provides a roadmap for combination immunotherapy in advanced ovarian cancer."]