For example, a study suggested that, in vitro, SIRT1 attenuated the stress response by modulating the JNK signaling pathway, probably via deacetylation of the JNK phosphatase, DUSP16 of AKI.887 A previous study found that SIRT1/p53 up-regulated modulator of apoptosis/FoxO3a deacetylation by depleting miR-183-3p could improve renal tubulointerstitial fibrosis after AKI.873 Furthermore, kidney ischemia/reperfusion injury, which is a major cause of AKI, is associated with decreased AMPK phosphorylation and a five-fold increase in kidney SIRT1 expression. The gene discussed is TP53; the disease is acute kidney injury.