Although we did not measure GLUT4 in the current study, one explanation for similar glucose disposal during the hyperinsulinemic clamp in the control and stroke survivors could be that GLUT4 expression or GLUT4 translocation was similar or greater in the stroke survivors which could serve to overcome the lower insulin-mediated glycogen synthase activity (i.e., “push” greater than “pull” mechanism [36]). This evidence concerns the gene INS and stroke disorder.