We hypothesize that the pharmacological inhibition of secreted KLKs, particularly KLK2, using the recombinant protease inhibitor MDPK67b, exerts an antitumor effect in PCa tumor cells in vitro by reducing proliferation and inducing apoptosis independently of the AR signaling and further modulates AR downstream targets such as PSA and PSMA providing a potential theranostic advantage in PCa. This evidence concerns the gene KLK3 and posterior cortical atrophy.