Indeed, Park et al. showed that myotubes derived from participants with severe obesity (BMI > 40 kg/m2) and with whole-body insulin resistance showed reduced activation of the AMPK pathway and downstream GLUT4 translocation to the plasma membrane in response to a 24 h EPS treatment compared to myotubes derived from lean and insulin-sensitive participants. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.