Overall the major findings from these challenging studies are 1) the ubiquitin-proteasomal degradation of hSphK1 is important in cell survival, 2) differential proteasomal degradation of hSphK1a and hSphK1b is cell-phenotype specific, 3) differential regulation of hSphK1a and hSphK1b may contribute to anti-SphK/S1P therapy resistance as demonstrated in prostate cancer cells [25, 26]. This evidence concerns the gene MBTPS1 and prostate cancer.