For example, Sphk1- but not Sphk2- is responsible for S1P export from breast cancer cells and S1P is linked to inflammation and cancer incolitis-associated cancer progression, while Sphk2 is linked to sensitization of human colon cancer cells to sodium butyrate-induced apoptosis; loss of Sphk1- not Sphk2- attenuates the development of intestinal inflammation and colitis-associated colorectal carcinogenesis [10,11,12]. This evidence concerns the gene SPHK1 and colonic neoplasm.