Given that SHP2 activity is believed to be dependent on Erk signaling, our study sets out to examine the hypothesis that the development of AKI following sequential exposure to hemorrhagic shock and sepsis, is mediated in part through dysregulated SHP2 activation resulting in stimulation of Erk1/2 as well as signal transducers and activators of transcription 3 (STAT3). This evidence concerns the gene MAPK3 and acute kidney injury.