For example, patients at risk of surgical site infection display an exacerbated MyD88 response after surgery,43,49 which was dampened by personalized prehabilitation, as we observed a reduction in mitogen-activated protein kinase-activated protein kinase 2 signaling in response to an exogenous stressor (TNF-α) in intermediate monocytes and protein kinase R-like endoplasmic reticulum kinase signaling in response to IL-2, 4, and 6 in classical monocytes and myeloid-derived suppressor cells. This evidence concerns the gene MAP2K2 and infection.