Our previous study [23] showed that knockdown of S1PR2 by the S1PR2 shRNA lentiviral vector suppressed p-PI3K, p-ERK, p-JNK, p-p38, and p-NF-κBp65 protein expressions 4 h after infection with Aa. To further elucidate which signaling pathways affected by JTE013 in regulating the immune response induced by Aa, we performed western blot analysis of BMMs treated either with vehicle or JTE013 (8 μM) with or without Aa infection for 4 h. The gene discussed is S1PR2; the disease is infection.