Notably, ALDH2 expression was found to be a default response to endotoxic stimulation, as its deficiency resulted in the accumulation of 4-HNE, suppression of the mitogen-activated protein kinase (MAPK) pathway, and the exacerbation of tubular epithelial cell apoptosis in LPS-induced AKI [141]. The gene discussed is ALDH2; the disease is acute kidney injury.