In a mouse colitis model, PCA can decrease both mRNA levels and protein concentration of Sphingosine kinases (SphK), which induces the phosphorylation of sphingosine to form sphingosine-1-phosphate (S1P), but increase the expression of S1P lyase (S1PL) which irreversibly degrade S1P, and thus, inhibit SphK/S1P pathway-mediated activation of the NF-κB pathway through S1P receptors (S1PR) [33]. The gene discussed is NFKB1; the disease is colitis.