We already reported that mild‐to‐moderate increases of IS (i.e. at concentrations up to 20 μM), as found during transition from mild to moderate CKD, promote monocyte differentiation towards macrophages with low‐inflammatory, pro‐fibrotic potential, through an AhR/NRF2‐HO1 signalling, sustaining chronic inflammation and maladaptive vascular remodelling.34 This evidence concerns the gene NFE2L2 and chronic kidney disease.