As there is indisputable evidence to support SphK2 compensatory mechanisms in the absence of SphK1 in ‘normal’ physiology (at least in mouse models) [19], and the discovery of SphK2 specific inhibitors (FTY720 and ABC294640), acting as competitive inhibitors of SphK2 (not SphK1), with the ability to be phosphorylated by SphK2 and be released from cells to act on S1P receptors, also suggests a wider functionality for this isozyme and its role in neoplasia and cancer [252, 253]. This evidence concerns the gene SPHK1 and neoplasm.