Nonetheless, several studies have provided evidence that the modulation of the SphK–S1P receptor axis influences the damage of proximal tubular cells, as well as the induction of AKI in mice (reviewed in [84]), leading to the assumptions that (a) renal ceramide levels did not solely account for the severity of proximal tubular damage and kidney injury severity and (b) SphK mutant mice might have altered renal S1P receptor expression profiles. Here, SPHK1 is linked to acute kidney injury.