The disease is primarily driven by Th2-associated cytokines such as interleukin (IL)-4, IL-13, and IL-31, which contribute to inflammation and exacerbate pruritus, perpetuating the "itch-scratch cycle." Recently, biologics targeting Th2 cytokines - such as dupilumab, lebrikizumab, and tralokinumab - have emerged as effective treatment options for moderate-to-severe AD. The gene discussed is IL4; the disease is Alzheimer disease.