On the other side, from an immunological perspective, it is widely accepted that the basis of atopic dermatitis lies in a type 2 inflammatory response initiated by keratinocyte stimulation and releasing alarmins: TSLP, interleukin (IL)-25 and IL-33, leading to ILC2 activation, with further IL-4, IL-5 and IL-13-driven Th2 and eosinophilic inflammation in the acute phase of AD, while Th1, Th17/Th22-mediated gamma interferon (γIFN) and IL-12 are predominant in chronic lesions [1,2,4,5,16,17,18,19,20,21,22,23,24]. The gene discussed is IL13; the disease is Alzheimer disease.