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Prostate cancers that recur after so-called androgen-ablation therapy ('CR-CaP') are typically more aggressive, more likely to spread to local lymph nodes and bones, and less likely to respond to second-tier treatments, and therefore, contribute to significantly decreased patient survival. We posit that enzymes called Src-family kinases (SFK) are required for the progression to CR-CaP, and thus, targeting these enzymes should prevent CR-CaP formation of suppress their growth. We will use animal models of human and mouse CR-CaP in conjunction with genetic and biochemical experiments to show that SFK are critical to the formation of CR-CaP, and thus, are therapeutically targetable using SFK-specific drugs. Our important pre-clinical studies on the critical role played by SFK in CR-CaP disease will serve as the foundation to establish immediate clinical trials in which CaP patients are treated with drugs such as KX2-391 at the commencement of androgen-deprivation therapy.