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Allergic responses are Th2- and IgE-mediated immune responses that evolved to protect against environmental substances and parasites. How-ever, these responses can also lead to allergy when inadvertently activated by noninfectious envi-ronmental antigens and cause harmful symptoms such as itching, inflammation, or tissue injury. As to our current understanding, mast cells are at the center of allergic responses (Galli et al., 2005; Bischoff, 2007). Mast cells are BM-derived hematopoietic cells localized under surfaces ex-posed to the external environment, such as the skin, airways, and intestine. They function as sentinel cells in host defense reactions includ-ing immediate hypersensitivity responses and allergic responses (Galli et al., 2005). Activated mast cells trigger allergic responses by releasing preformed granule-associated chemical media-tors, producing multiple cytokines and che-mokines, and secreting de novo synthesized arachidonic acid metabolites and various pro-teins (Metcalfe et al., 1997; Bischoff, 2007). Mast cells recognize antigens via IgE and specific Fc receptors, termed FcRI. Binding of multivalent antigen to FcRI-bound IgE in-duces receptor aggregation and triggers mast cell activation (Kinet, 1999; Siraganian, 2003). FcRI is expressed on the surface of mast cell as a tetrameric complex consisting of an IgE-binding subunit, a signal-modulating subunit, and two signal-transduction subunits (Kraft and Kinet, 2007). The signaling cascades elicited by FcRI aggregation in mast cells have been ex-tensively studied (Kalesnikoff and Galli, 2008). Briefly, the conserved immunoreceptor tyrosine-based activation motifs (ITAMs) within the cyto-plasmic tails of the and subunits are rapidly phosphorylated upon FcRI stimulation in a Lyn-dependent manner (Garman et al., 1999