In the present study, we used a renal damage model based on folic acid (FA) [31] on transgenic mice and cultured human tubular epithelial cells HK2 with ILK depletion [7] to investigate the role of ILK and downstream intracellular mechanisms involved in mitochondrial dysfunction during AKI-to-CKD transition. The gene discussed is ILK; the disease is chronic kidney disease.