It is plausible that 1α,25(OH)2D3-mediated suppression of tumor-specific actin-binding molecules (i.e., ANLN and ECT2) could be utilized in combination with FDA-approved chemotherapeutics that target actin cytoskeletal dynamics and RhoA signaling to improve treatment response outcomes in PCa patients. This evidence concerns the gene ECT2 and posterior cortical atrophy.