Therefore, this study was designed, using the sickle cell mouse model, to: 1) investigate the pathogenic mechanisms in the penis causing endothelial NO/cGMP/PKG/PDE5 derangements that predispose priapism, and 2) identify a pharmacologic mechanism by which PDE5 inhibitors potentially serve as a therapy for priapism related to SCD. Here, PRKG1 is linked to Schnyder corneal dystrophy.