It has been reported that SphK1 is 15-fold higher than SphK2 in normal humans, whereas in platelets from sepsis patients, SphK1 expression is significantly reduced with no change in SphK2 Recent studies indicate that platelets produce a large amount of S1P through de novo synthesis, which is released after platelet activation, thereby modulating local cellular responses (57). The gene discussed is SPHK1; the disease is Sepsis.