A limitation of our study was the use of a whole-body double KO model for Ctns and Nlrp2. Therefore, we cannot exclude that amelioration/delay in kidney damage we documented in Ctns-/- Nlrp2-/- mice are indirect as changes in other tissues, or cells other than PTEC, may have an effect on kidney disease progression. This evidence concerns the gene CTNS and Nephropathy.