Interestingly, recent clinical observations have suggested an inverse relationship between SPL and SphK1 activities on the level of S1P in prostate cancer specimens implying that the overall increased S1P level commonly observed in cancer does not merely reflect overexpression of SphK1 activity, but could also be a consequence of loss of SPL expression [21]. The gene discussed is SPHK1; the disease is Familial prostate cancer.