Taken together with numerous reports demonstrating that acutely increasing circulating NEFA concentrations causes skeletal muscle insulin resistance and that insulin resistance has plateaued by 24 h of forearm immobilization (11), this would suggest that acutely increasing circulating NEFA causes insulin resistance via a different, albeit transient, mechanism to a lack of contraction per se (e.g., Randle Cycle vs. reduced GLUT4 translocation, respectively; Refs. The gene discussed is SLC2A4; the disease is Insulin resistance.