The aggregation of high-affinity immunoglobulin E (IgE) receptors (Fc[epsilon]RI) on mast cells is a critical event in the initiation of an allergic reaction. Coengagement of Fc[epsilon]RI with immunoglobulin G (IgG) low-affinity receptor Fc[gamma]RIIB/CD32 inhibits degranulation and the release of inflammatory mediators from mast cells and has therefore been proposed as a new therapeutic approach for the treatment of allergies. In this study, we investigated whether Fc[gamma]RIIB, besides inhibiting degranulation, negatively regulates other signalling pathways downstream of Fc[epsilon]RI. For this, we determined the phosphorylation and/or expression of proteins involved in the regulation of mast-cell apoptosis. Coaggregation led to an attenuation of Akt phosphorylation but did not inhibit phosphorylation of transcription factor Foxo3a or its proapoptotic target, Bim. Similarly, Fc[epsilon]RI-dependent expression of the prosurvival gene A1 was not affected by coaggregation. Our data demonstrate that coengagement of Fc[epsilon]RI and Fc[gamma]RIIB inhibits degranulation but not the signalling pathways regulating Bcl-2 family members Bim and A1.