IL1B and acute kidney injury: The activation of these molecules can result in the secretion of pro‐inflammatory cytokines, namely pro‐IL‐1β and pro‐IL‐18,[24, 25, 26] in turn, driving the infiltration of a large number of immune cells into the kidney tissues.[27, 28, 29] For example, in the early stages of AKI, damaged TECs can promote the differentiation of M1 macrophages through the release of exosomal miRNAs.