However, the demonstration in the present study that loss of either MrgprB2 or β-arr2 in MCs results in decreased MC recruitment, cytokine generation, and AAI suggests that β-arr2-biased signaling via MrgprB2 contributes to the pathogenesis of allergic asthma and provides a novel target for modulating experimental disease phenotype in mice. This evidence concerns the gene ARRB2 and allergic asthma.