In the cardiovascular system, in infarcted rat hearts, dapagliflozin treatment after infarction increases myocardial M2 macrophage polarization with a concomitant decrease in M1 via acute-phase response factor (STAT3) signaling, a well-known key factor in the polarization of M2, contributing to attenuate cardiac fibrosis [168,169]. The gene discussed is STAT3; the disease is infarction.