Recently, it was suggested that IL-4 and IL-13 promote the neurogenic itch, which is the hallmark of AD, via two non-histaminergic pathways: directly, by stimulating itch sensory neurons, and indirectly, via interaction with the IL-31 pathway, a well-known pruritogenic cytokine, through up-regulation of the IL-31 receptor in keratinocytes and dorsal root ganglia [23,24]. This evidence concerns the gene IL4 and Alzheimer disease.