To assess the potential clinical utility of targeting B7H3 as a treatment strategy for advanced prostate cancer, we evaluated the transcript abundance of B7H3 and other previously studied cell surface targets — PSMA, PSCA, TROP2, STEAP1, and CEACAM5 — in 185 tumors from 98 patients with treatment refractory mPC and across a panel of 26 mPC PDX and organoid models representing the genomic and phenotypic heterogeneity of patient tumors. This evidence concerns the gene CEACAM5 and Familial prostate cancer.