Prostate tumors of Pten/Trp53 mice displayed increased Skp2–Foxa1–Pcna signaling and colocalization, whereas disruption of the Skp2–Foxa1 interplay in Pten/Trp53/Skp2 triple‐null mice demonstrated decreased Pcna levels and increased expression of Foxa1 and luminal positive cells. The gene discussed is FOXA1; the disease is prostate neoplasm.