As to the nature of mechanism behind the increased RBC S1P content in diabetes, it may be due to the higher Sphk1 activity we have observed in diabetic RBC and perhaps to less active Mfsd2b restricting S1P efflux as its function is hampered by high intracellular pH25, a characteristic feature of diabetic RBC48. Here, MFSD2B is linked to diabetes mellitus.