Although the low affinity (FcεRII/CD23) receptor has also been described in ASM cells with enhanced signal in ASM tissue from asthma[29], and Roth et al. have suggested the involvement of both FcεRII/CD23 and FcεRI in IgE-induced ASM remodeling[16]; presently observed proliferative effect of IgE appear to primarily involve FcεRI since the lentiviral shRNA-mediated inhibition of spleen tyrosine kinase (Syk), a signature kinase in FcεRI signaling[22], abolished the IgE-induced HASM proliferation. The gene discussed is IGHE; the disease is asthma.