We have long argued [62, 63] that highly conserved proteins such as cyclic nucleotide phosphodiesterases (PDEs) potentially make excellent drug targets in neglected diseases because of the shortcuts in development time and money this approach affords, drawing as it does on the wealth of pharmacological, genetic, structural and toxicological information available on PDE inhibitors for the treatment of conditions as diverse as heart failure [64], erectile dysfunction [65] and chronic obstructive pulmonary disorder (COPD) [66]. The gene discussed is ALDH7A1; the disease is erectile dysfunction.