Considering a strong correlation between un-coupled NOS3 and CSF1-CSF1R signaling and the inhibitory impact of both GSNO and CSF1R blockade against M1-M2 dichotomy, we hypothesized that GSNO could potentially S-nitrosylate CSF1R to inhibit CRPC tumor burden, overall oxidation, and macrophage dichotomy. Here, NOS3 is linked to neoplasm.