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Mechanistically, PKC blockade destabilizes XIAP, relieving caspase inhibition, stabilizing PTEN, and suppressing Wnt\/\u03b2-Catenin-ATF3 signaling to drive CCL4 expression. In resistant models, PKC inhibition synergizes more effectively with anti-CTLA-4 than with anti-PD-1\/PD-L1, in association with reduced intratumoral regulatory T cells and reinforcement of CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cell effector function. These findings define the PKC\u2013XIAP axis as a central regulator of immune resistance and provide a mechanistic rationale for PKC inhibition plus anti-CTLA-4 as a salvage strategy in ICB-refractory cancers.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2600501123","type":"journal-article","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T16:10:26Z","timestamp":1780503026000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":0,"title":["Targeting XIAP-coordinated PKC signaling resensitizes PD-1-refractory tumors for rechallenge"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1817-7771","authenticated-orcid":false,"given":"Jupeng","family":"Yuan","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05jb9pq57","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Shandong Provincial Key Laboratory of Precision Oncology, Shandong Cancer Hospital and 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