IL6ST and Eczematoid dermatitis: The discoveries of individuals with complete gp130-deficiency due to null/nonsense bi-allelic mutations of IL6ST [11], or pathogenic dominant-negative heterozygous variants of IL6ST [9], and a phenotype of eczema, hyper-IgE, and eosinophilia, likely explain these features of autosomal dominant hyper-IgE syndrome due to STAT3 negative dominance [61] and further highlight the role of IL-6 signaling in restraining atopic and allergic responses.