Second, we show that Mcl-1 overexpression reduces eosinophil death both in vitro and in vivo in the context of airway allergy, extending our previous observations that Mcl-1 is a key regulator of neutrophil apoptosis,9 11 and that CDKi induce eosinophil apoptosis concurrent with Mcl-1 loss.12 While cytokine-mediated changes or maintenance in eosinophil Mcl-1 (by IFN-γ and IL-5) have previously been reported, this is to our knowledge the first report that Mcl-1 aggravates allergic airway inflammation in vivo. This evidence concerns the gene IFNG and allergic respiratory disease.