However, the results are complex and at times difficult to reconcile: while a pharmacological S1PR1 antagonist had no effect in LDLR−/− mice [16], an S1PR1 agonist reduced atherosclerosis [17]; endothelial-specific S1PR1 deletion enhanced [18], global S1PR2 deficiency suppressed [19], whereas S1P3R had no effect on atherosclerosis albeit altered plaque composition [20]. The gene discussed is S1PR2; the disease is atherosclerosis.