The observations regarding the mechanisms triggered by AKI point to an age-related magnification of several proinflammatory-related processes, including gene overexpression of some proinflammatory factors (Lcn-2, Cxcl1, and Il-6), overactivation of inflammatory-cell-death pathways such as necroptosis, and amplification of cellular senescence including immunosenescence (Figure 10). The gene discussed is CXCL1; the disease is acute kidney injury.