The NKX3.1 cancer-associated variants R52C or T64A, present in 14% and 11% of the population, respectively, impair the mitochondrial function of NKX3.1 and lead to the dysfunction of mitochondrial OXPHOS and promotion of aerobic glycolysis which can result in a more aggressive early PCa phenotype. The gene discussed is NKX3-1; the disease is posterior cortical atrophy.