In insulin-resistant female diabetic mice, increased myocardial expression of SGK1 and ENaC caused myocardial fibrosis and eccentric LV hypertrophy, while empagliflozin reduced SGK1 and ENaC levels, as well as related pro-fibrotic signals, leading to an improved diastolic relaxation. The gene discussed is SGK1; the disease is Myocardial fibrosis.