PCa showing a high tumor mutational burden, high programmed cell death protein 1 (PD-L1) tumor expression, cyclin-dependent kinase 12 (CDK12) mutations, mismatch repair-deficient (dMMR), a high microsatellite instability, homologous recombination deficiency, and (BRCA2 and ATM) POLE/POLD1 mutations, as well as patients in a good status of health, provide ideal candidates for immunotherapy because these changes increase response to immunotherapy by increasing the tumor mutation burden and neoantigen expression [36,37,38]. The gene discussed is PDCD1; the disease is posterior cortical atrophy.