Although the experimental treatment of Ara C does not represent a real pathogenesis process and a direct test in patients is not feasible, results from aforementioned experimental models provide evidence to support the role of TP53 loss in promoting prostate cancer cells’ genome instability and the arising of androgen-independent cell growth, either via increasing the number of cells with CNVs and/or promoting a higher incidence of CNVs in a given number of cells. The gene discussed is TP53; the disease is prostate carcinoma.