To our surprise, despite the fact that AR has a cross-talk role with TGF-β signaling and plays an important role in the development and progression of PCa and its androgen-independent transformation [35], we confirmed that TGF-β regulates the gene expression of SPOP via SMAD3 in both androgen-independent (DU145, PC3) cell lines and androgen-dependent (LNCaP) cell line (Figures 2D, 2E, Supplementary Figure 2A and 2B). The gene discussed is AR; the disease is posterior cortical atrophy.