In this regard, in nephrotoxic AKI induced by a folic acid overdose, a model that shares the main pathogenic processes of cell death and proliferation, inflammation and fibrosis with human AKI, results suggest that QM56 may improve renal function and tissue injury evaluated by classical clinical parameters, as well as through expression of more reliable biomarkers of AKI such as Kim-1 and Ngal [2], [26], [27]. The gene discussed is HAVCR1; the disease is acute kidney injury.