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Background and Objective: Priapism is a disorder of uncontrolled,prolonged penile erection unassociated with sexual purpose or desire,having significant clinical implications.Ischemic priapism,the most common variant,occurs with high prevalence in patients with sickle cell disease.Management of recurrent ischemic priapism remains vexatious for many clinicians and historically has mainly consisted of reactive treatments rather than preventative strategies.New insights surrounding the molecular mechanisms underlying this disorder have suggested the opportunity to develop new therapeutic targets.This presentation serves to review recently described molecular mechanisms involved in the pathophysiology of priapism.Methods: Systematic literature review of scientific studies pertaining to priapism.Results: Several molecular mechanisms are now identified to be involved in the pathophysiology of recurrent ischemic priapism,principally that involving dysregulation of nitric oxide signaling.Conclusions: The molecular basis of recurrent ischemic priapism has been increasingly refined based on emerging scientific progress in this field.Early evidence exists for the use of molecular effectors of the nitric oxide signaling pathway.