KEAP1 and chronic kidney disease: Therefore, the aims of this study were to i) identify the site of acute tubule injury upon Cul3 deletion and to characterize the time-course of its transition into CKD, thus, establishing KS-Cul3−/− mice as a novel genetic CKD model; ii) test the hypothesis that dysregulation of the cell cycle and Keap1/Nrf2 pathway precedes tubule injury, and that the cyclin E inhibitor roscovitine ameliorates kidney injury; iii) test the hypothesis that CUL3 plays a broader role in kidney disease by examining CUL3 expression in mouse models of AKI and CKD, and in fibrotic human samples.