We thus propose that each cancer subclone achieved lower pro-apoptotic C16 Cer and higher pro-inflammatory S1P signaling (Figure 7, Supplementary Figure 9) through a combination of greater SK1 protein expression and/or increased SK1 activity levels through ERK2 mediated phosphorylation (Figure 6A, 6B). The gene discussed is SPHK1; the disease is cancer.