Mechanistic studies reported that both myocardial FNDC5 overexpression and exogenous irisin administration attenuated cardiac adverse structural remodeling due to diabetes, including myocardial fibrosis, and that its protective effects were closely associated with activation of integrin αVβ5-AKT signaling and attenuation of oxidative/nitrosative stress (Lin et al., 2021). The gene discussed is FNDC5; the disease is Myocardial fibrosis.