The etiopathogenesis of atopic dermatitis (AD) is complex, and it is still unclear whether the initial symptoms of dermatitis are due to a dysfunction of the epidermal barrier, including a deficiency in filaggrin, loricrin, involucrin proteins, and an imbalance between the production of proteases and antiproteases in the stratum spinosum (the “outside-in” hypothesis) or immune dysregulation related to the innate and acquired Th-2 response (the “inside-out” hypothesis) [45]. The gene discussed is IVL; the disease is atopic eczema.