Studies have shown that using S1PR1 shRNA, a G protein-coupled receptor for S1P or FTY720, an antagonist of S1P that is used clinically for other indications, inhibits S1PR1 expression and downregulates STAT3 activity, causing growth inhibition of the B-cell lymphoma tumor cells in vitro and in vivo (80). This evidence concerns the gene S1PR1 and neoplasm.