Several lines of evidence link the oncogenic role of S1P to the activity of SphK1: (i) SphK 1 and S1P levels regulate drug and radiation resistance in cell cultures; (ii) overexpression of SphK1 and an increase in S1P levels drive tumors toward more aggressive forms in animal models, while SphK1 inhibition restores drug and radiation sensitivity; (iii) SphK1 is overexpressed in many types of tumor, and it has been shown that high levels of SphK1 directly correlate with poor survival in patients. This evidence concerns the gene SPHK1 and neoplasm.