Taken together, these findings and the local expression of both CCL20 and its receptor CCR6 argue in favour of the potential role of CCL20 in kidney disease pathophysiology, although the precise role remains unclear, given the contradictory preclinical evidence in AKI resulting from different triggers [15,16] and the lack of association with long-term hard outcomes in the present cohorts treated according to clinical guidelines. This evidence concerns the gene CCL20 and kidney disorder.