Human heart tissue from diabetic patients with heart failure recapitulated the in vitro findings with human diabetic failing heart tissue exhibiting reduced miR126 and increased ADAM9 expression with a reduction in phosphorylated MerTK, a surrogate marker for MerTK signaling, indicating that antagonism of MerTK-mediated processes under diabetic conditions could translate to an increase in adverse clinical outcomes in heart failure patients. The gene discussed is ADAM9; the disease is heart failure.