Chronic itch in inflammatory skin diseases, such as atopic dermatitis, markedly diminishes the quality of life of affected individuals. Comprehensive progress has been made in understanding itch signaling and associated mediators in the skin, dorsal root ganglia, spinal cord, and central nervous system, which may amplify or suppress atopic itch. Conventional therapies for atopic dermatitis are capable of reducing atopic itch; however, most patients are not satisfied with the antipruritic capacity of conventional treatments. Exploring itch pathways and mechanisms may lead to novel therapeutic approaches for atopic itch.