However, PBMCs from people with hyperimmunoglobulin E syndrome, who are predisposed to S. aureus infections, produce less IFNγ upon stimulation with heat-killed S. aureus or with IL-12 and IL-18 but have frequencies of Candida albicans-specific IFNγ-producing CD4 T-cells comparable to healthy volunteers [9, 25]. The gene discussed is CD4; the disease is hyper-IgE syndrome.