The data show that the likelihood of ED occurring within 10 years in people diagnosed with diabetes is 50%, and its severity as well as prevalence is significantly correlated with factors such as age duration at the time of diabetes, type of diabetes, glycemic control, diabetic neuropathy, diabetic nephropathy and hypertension. First, let’s look at how the male sexual response occurs. In the first step, desire is generated; in the second step, nerve signals are transmitted; in the third step, blood vessels are filled with blood and impulses are generated. And diabetes can affect male function in three ways, namely vascular, neurological, endocrine and psychological, including almost all causes of organic ED. First, 70% of people on the diabetic ED have vascular lesions, including large-vessel, small-vessel and microvascular lesions, affecting local vascular congestion. Second, diabetic-induced neuropathy and neurotransmitter changes are central to ED. In particular, peripheral nerve (autonomic nerve) lesions are predominant. Such as affecting sensory nerve conduction, affecting the concentration of neurotransmitters, especially NO concentration, which is the most important neurotransmitter affecting the sexual response. In addition, sympathetic neuropathy caused by diabetes can lead to local venous leakage, which can cause dysfunction. As well as the endocrine changes caused by diabetes, a decrease in the concentration of androgens (testosterone) in the serum can lead to ED! Clinically, phosphodiesterase (PDE5) inhibitors are the first-line drugs for the treatment of diabetic ED, achieving and maintaining satisfactory erectile capacity, even in patients with poor glycemic control and severe complications, in addition to combined androgen supplementation in some patients.