In a retrospective series of 66 adult patients with recurrent GBM treated with PD-1 inhibitors (pembrolizumab or nivolumab), including 17 long-term responders, genomic and transcriptomic analysis revealed a significant enrichment of phosphatase and tensin homolog (PTEN) mutations associated with immunosuppressive expression signatures in non-responders (p < 0.05), and enrichment of mitogen-activated protein kinase (MAPK) pathway alterations (protein tyrosine phosphatase non-receptor type 11, BRAF) in responders (p < 0.05). The gene discussed is PDCD1; the disease is glioblastoma.