In vitro studies demonstrated elevated levels of H3K9ac in the promoters of Notch1 and Notch4 in hyperglycemia-treated podocytes, whereas Sirt6 suppressed Notch1 and Notch4 transcription by deacetylating histone H3K9 and protected podocytes from apoptosis and inflammation through inhibition of the Notch pathway [33]. The gene discussed is NOTCH1; the disease is Hyperglycemia.