To further investigate the contribution of tumor‐intrinsic METTL5 to immune resistance beyond regulation of immune cell recruitment, we utilized data from a published ICB‐cohort[30] from TNBC tumors, which are similar to OC at the molecular level.[45] Upregulated differentially expressed genes (DEGs) identified in ICB responders and nonresponders in the TNBC cohort were used to define the responder gene set and the nonresponder gene set, respectively (Table S6, Supporting Information). This evidence concerns the gene METTL5 and neoplasm.