For example, β-catenin/CBP-dependent signaling has been implicated in AD pathogenesis and its inhibition prevents hapten-induced AD-like symptoms (78), activation of NRF2 signaling has been found therapeutic in AD (79), high levels of proangiogenic VEGFA are seen in AD patients (80), decreased levels of EGFR are seen in AD lesional skin (81), quercetin has been shown to inhibit MMP9 along with ERK1/2 and NF-κB pathways in AD model of human keratinocytes (82). The gene discussed is NFKB1; the disease is Alzheimer disease.