Ni application caused barrier defects by reduction of terminal differentiation (filaggrin (FLG), FLG2, loricrin (LOR), and late cornified envelope proteins (LCEs)), tight junction (claudin (CLDN)1/CLDN8), and lipid metabolism (fatty acid 2-hydroxylase (FA2H), fatty acid binding protein 7, brain (FABP7)) AD-related markers [73]. The gene discussed is FABP7; the disease is Alzheimer disease.