These pathogenic variants skew T-helper cell differentiation towards a Th2 phenotype, increasing IL-4, IL-13, and IFN production, exacerbating allergic responses, and resulting in severe eosinophilia and multiple allergic conditions, like severe atopic dermatitis, asthma, and food allergies, in addition to failure to thrive, autoimmune thyroiditis, elevated eosinophil counts, gastrointestinal disease, and hypothyroidism [15,54,55]. This evidence concerns the gene IL4 and atopic eczema.