The fact that tadalafil reversed age-related PDE11A4 ghost axons at a 10 μM brain exposure (i.e., 110 mg/kg) but not a 1 μM brain exposure (i.e., 11 mg/kg) suggests that this effect of tadalafil is mediated via it binding to PDE11A4, as opposed to inhibiting PDE5 since much lower plasma exposures of tadalafil are required for treating erectile dysfunction [77]. This evidence concerns the gene PDE5A and erectile dysfunction.