Importantly, therefore given the protection afforded by ES-62 in acute and chronic models of asthma, our studies have identified that the differential cytokine responses in serosal (PDMC) and mucosal (BMMC) mast cell subsets shaped by complex interactions of ST2, FcεRI and LPS/TLR4 signals can be modulated by ES-62 via both ST2-dependent and independent mechanisms. The gene discussed is TLR4; the disease is asthma.