Taken together, our study is aimed to investigate: (1) whether Grb2 is affected by AKI and consequently triggers cardiac dysfunction in CRS-3, (2) what the upstream molecular mechanism underlying Grb2-triggered cardiomyocyte damage is, and (3) what the intracellular events in response to Grb2 upregulation during AKI are. This evidence concerns the gene GRB2 and acute kidney injury.