For example, with low levels of STAT3 shifting the latent–lytic balance towards the lytic state, and STAT3 transcriptionally regulating SZF1 levels, it was not surprising to find that patients with the primary immunodeficiency disease, known as Job’s syndrome (or autosomal dominant hyper-IgE syndrome), who have a dominant negative mutation in their STAT3 gene, exhibit higher levels of spontaneously lytic cells. This evidence concerns the gene STAT3 and Autosomal dominant hyper-IgE syndrome.