Our data suggest that the decrease in circulating S1P during PCa progression may stem from a highly significant downregulation of erythrocyte sphingosine kinase-1 (SphK1) activity (2.14±0.17 pmol per mg protein per minute in PCa patients vs 4.7±0.42 in healthy individuals, P<0.0001), which may be a potential mechanism of cancer-induced anaemia. The gene discussed is SPHK1; the disease is posterior cortical atrophy.