Previous data have demonstrated that, in a model of chronic kidney disease, LCN2 stimulates the recycling of activated EGFR to the cell border (Yammine et al., 2019), leading to increased EGFR activity; importantly, this is independent of LCN2 secretion as an LCN2 mutant that is not secreted can still stimulate the recycling of EGFR. This evidence concerns the gene EGFR and chronic kidney disease.