In other studies, as in human atopic dermatitis (AD), IFN-γ was described as a driver of chronic inflammation, and its overexpression can lead to recurrent inflammation and pruritus, causing lichenoid degeneration of the skin in the chronic phase (48, 49) and, as such, may also have a role in the lichenification process of IBH. This evidence concerns the gene IFNG and atopic eczema.