Here, through transgenic rats harboring the hKLK1 gene, we initially demonstrated that hKLK1 could preserve the erectile function in DM rats by inhibition of excessive OS and apoptosis, correction of cavernous histologic abnormalities, and activation of PI3K/AKT/eNOS signaling to generate more cGMP in vivo and in vitro (shown in Figure 9). The gene discussed is AKT1; the disease is diabetes mellitus.