Regarding a particular Cer, pancreatic adenocarcinoma subclones which displayed increased proliferation were characterized by high S1P/C16:0-Cer ratios compared to an origin control cell line [28]; consistently with the S1P/Cer rheostat hypothesis, the inhibition of S1P synthesis reduced S1P/C16:0-Cer, inhibited proliferation, and increased apoptosis. Here, CBLN1 is linked to pancreatic adenocarcinoma.