While there is no marked inhibition of IL-17A or IL-22 with this IL-4 receptor-α antagonist, there is a marked decrease in IL-17-related products (elafin/PI3, IL-23p19/IL23A, and S100A8), with parallel increases in barrier genes (CLDN8 and CLDN11) [24], and a trend towards increases in expression of differentiation genes such as FLG and LOR. Interestingly, an overall exacerbation of the inflammatory lesional AD phenotype was observed in the placebo-treated cohort, despite “clinical improvements” seen in these patients, further confirming the importance of biomarker studies in AD [24]. This evidence concerns the gene CLDN11 and Alzheimer disease.