As such, they control cell fate by regulating the relative amounts of pro-apoptotic Cer and Sph to pro-survival S1P.6 S1P acts extracellularly as a ligand to S1P receptors, leading to increased tumor cell migration and proliferation.7,8 Thus, blocking SK with a specific inhibitor would not only decrease the levels of S1P and hence tumor migration, but also lead to an increase in Cer and Sph, thereby inducing cell death. The gene discussed is CBLN1; the disease is neoplasm.