Consistent with the observed effects of FGF21D2D3 on DCM in vivo, we found that FGF21D2D3 treatment led to greater phosphorylation and activation of FGFR1 and AMPK than FGF21WT, both of which were suppressed by high glucose (HG) and palmitic acid (PA) in H9c2 cardiomyocytes (Figure 6C,D). The gene discussed is FGFR1; the disease is familial dilated cardiomyopathy.