In this regard, Faubel et al. have advanced the following hypothesis (Andres‐Hernando et al., 2017; Soranno et al., 2016): (a) AKI causes renal IL‐6 synthesis; (b) renal release of IL‐6 stimulates splenic immune cell IL‐10 production; and (c) with splenic IL‐10 release, an “organ cross talk” loop is completed as spleen‐derived IL‐10 inhibits AKI‐triggered inflammation/AKI severity. This evidence concerns the gene IL10 and acute kidney injury.