TNFRSF12A and acute kidney injury: We identify repression of Fn14, but not that of CYLD, as the central mechanism whereby miR-19a exerts tubular protection during septic AKI because in vitro cellular experiments demonstrate that miR-19a attenuates the LPS-inducible reduction in cell survival, enhancement in DEVDase activity, and elevation in TUNEL- as well as cleaved caspase-3-positive staining.