Abstract The BCR-triggered responses of mature and transitional immature B cells differ at both the biochemical and functional level. It was previously shown that BCR cross-linking in vitro results in death of early transitional (T1) immature B cells whereas mature B cells survive and start proliferation. In this study, we show that in Ch1 cell line which are a model system for immature mouse B cells, Surface IgM (sIgM) cross-linking leads to cell cycle arrest. we found that this immature B cells do enter, but fail to completely progress through G1 phase of the cell cycle following BCR engagement. Interestingly, IL-4, which by itself does not stimulate proliferation of immature B cells, could rescue these cells from G0 /G1 arrest. Consistent with this idea, IL-4 can reverse effect of anti-Ig Abs to promote cell cycle progression of immature B cells. To investigate the different signaling pathways involved in these processes, CH1 cells were stimulated with anti-IgM alone, with IL4 alone, or with a combination of both IL4 and anti-IgM. Following this western blot strategy, protein/DNA transcription factor arrays and microarray data were employed to monitor the evolution of the signaling cascades. we have analysed the role of the MAP kinase families (MAPK) cascades, which are required for growth-factor-stimulated replication and for differentiation of B cells. All the intermediate signal transducers and the distal transcription modulators were studied to understand how intracellular signals from these two distinct receptors integrate to make the conesquence cell-fate decision.