To further demonstrate that non-DNMT3A-CHIP is causally associated with AKI and delineate disease mechanisms, we focused on CHIP caused by inactivating mutations in TET2 and JAK2 p.V617F, which made up more than 35% of non-DNMT3A-CHIP cases in our study and are each independently associated with AKI risk. This evidence concerns the gene TET2 and acute kidney injury.