Figure 1. S1P activated by SphK1 is the driver of persistent NFκB and STAT3 activation linked to tumorigenesis during CAC. (A) Increased levels of SphK1 and S1P during colitis lead to a feed-forward amplification loop driving persistent NFκB and STAT3 activation in tumors, tipping the balance toward growth/progression. (B) Inhibition of S1P signaling by the mimetic FTY720, abolishes persistent NFκB and STAT3 activation, suppressing development and progression of tumors during CAC.