Although a number of cell surface markers including CD86, CD80, and CD40 increase in expression as DC undergo maturation (a process that confers the ability to deliver ‘signal 2’ in order to activate T cells and generate a range of effector responses [3]), we chose to focus on the expression of CD86 since upregulation of this costimulatory molecule is closely linked to competence for T cell activation and the development of airway hyper-responsiveness in an animal model of asthma [30]. The gene discussed is CD40; the disease is asthma.