We hypothesized that ERG− tumor cells might evoke similar tumor microenvironment responses and found common transcriptional pathways that were upregulated in the tumor, stroma, and CD4 T-cell populations of ERG− patients, including the PD-1 and interferon-gamma signaling pathway, suggesting that ERG- tumor cells may give rise to a distinct immune cell niche and tumor microenvironment. The gene discussed is PDCD1; the disease is neoplasm.