The pathogenesis of cisplatin-induced AKI is mostly attributable to the metabolic activation of cisplatin into a highly reactive substance that causes oxidative stress by disrupting the antioxidant system, producing inflammatory mediators (such as TNF-α, ICAM-1, and MCP1), leukocyte infiltration, endoplasmic reticulum stress, and apoptotic cell death [38, 39]. The gene discussed is CCL2; the disease is acute kidney injury.