SPL inhibition by THI with subsequent increase in circulatory and cardiac levels of S1P and its endogenous analogue dhS1P resulted in improved resuscitation and survival rates after cardiac arrest in SphK1 knockout (SphK1-KO) mice; moreover, the inhibition of SPL with THI in the same animals restored reduced gene expression of S1PR2 and partially recovered decreased mRNA level of S1PR1 in the heart [131]. This evidence concerns the gene SGPL1 and cardiac arrest.