Therefore, even if sotagliflozin is able to inhibit myocardial SGLT-1, its role in restoring intracellular substrate utilization (including restored GLUT-4-mediated glucose uptake) is expected to prevail over the possible negative effect of SGLT-1 inhibition due to the reduction of glucose myocardial substrate with a consequent less viability in response to ischemia. Here, SLC5A1 is linked to ischemia.