These results suggest that keratinocyte-specific high expression of WFDC12 may up-regulate the expression of ALOX12 and ALOX15 and promote the accumulation of inflammatory mediators 12-HETE and 15-HETE of AA metabolites by activating the lipoxygenase AlOX12/15 pathway in the epidermal AA metabolic pathway, thus aggravating those AD symptoms induced by DNFB in mice. Here, ALOX12 is linked to Alzheimer disease.