The inverse relationships between miR-96 and RARγ were robust and significant across cell models, murine PCa models and clinical cohorts, and equal or greater than with previously identified targets including FOXO1. Biochemical tests established that miR-96 binds directly to multiple target sites contained within the 3′UTR of RARG, and using the bi-miR capture approach revealed ~400 direct targets enriched for predicted miR-96 target sequences, and identified targets were directly bound and downregulated upon miR-96 overexpression. The gene discussed is FOXO1; the disease is posterior cortical atrophy.