These primary immunodeficiencies involve defects in neutrophils/polymorphonuclear cells (PMNs); patients with CGD have defects in proteins of the NADPH oxidase system which lead to reduced production of microbicidal ROS by PMNs [1], individuals with hyperimmunoglobulin E syndromes suffer from defective neutrophil chemotaxis resulting from decreased production of IFN-γ by their T lymphocytes [2] and patients with osteopetrosis have defective leukocytic-ROS production in addition to problems with bone resorption [3]. This evidence concerns the gene IFNG and hyper-IgE syndrome.