PTEN loss activates PI3K–AKT signaling, and mTORC1 stimulates pyrimidine synthesis through S6K1-mediated CAD phosphorylation. This exploratory public-data analysis tested whether PTEN deletion in primary prostate cancer is associated with CAD, mTORC1 and pyrimidine-synthesis expression, and whether these survive protein-level and confounder analyses. In 485 primary tumors from The Cancer Genome Atlas Prostate Adenocarcinoma (TCGA-PRAD; 159 PTEN-deleted), deletion was associated with higher CAD mRNA (Hedges’ g = 0.57) and higher Hallmark mTORC1 scores (g = 0.54). In 342 tumors with reverse-phase protein-array data, deletion was accompanied by lower PTEN protein and higher AKT Ser473 phosphorylation but not by a higher pre-specified mTORC1 phospho-output composite (g = −0.02), itself uncorrelated with the transcriptional score. In a pre-specified model adding purity, TP53, RB1, ERG fusion and batch (n = 276), the PTEN–CAD association was absent (β = −0.002; p = 0.96), whereas the mTORC1-score association persisted. In a post hoc decomposition, ERG fusion, which co-occurs with PTEN deletion (odds ratio 3.6), changed the coefficient most. Across eight cohorts, a small PTEN mRNA–CAD association (g = 0.23) was attenuated to 0.14 after ERG adjustment, with overlapping confidence intervals (Hartung–Knapp p = 0.071). Bulk-tumor pathway signatures and PTEN–CAD associations need protein-level and ERG-aware interpretation.