Due to the fact that pressure overload (TAC) fails to induce pathological hypertrophy, myocardial fibrosis, LV dilation and dysfunction in mice with global SGLT1 knockout [3], the upregulation of SGLT1 seems to be causally implicated in adverse remodeling in response to chronic hemodynamic overload. This evidence concerns the gene SLC5A1 and Myocardial fibrosis.