 Atopic Dermatitis AD is thought to be mediated by Th2 type T cells elaborating a number of cytokines which are blocked in vitro by apremilast. The chronic Atopic Dermatitis AD pathway may involve a change to Th1 cytokines. Genetic factors do not contribute as much to the course of Allergic Contact Dermatitis ACD as in Atopic Dermatitis AD. Rather, Allergic Contact Dermatitis ACD is a type IV, T-cell mediated, delayed-hypersensitivity reaction that can be self-limited. Similar to Atopic Dermatitis AD, a number of pro-inflammatory cytokines are involved in recruiting T cells preferentially to the skin: Th1 cytokines, Th2 cytokines, CD8 cytokines, and T-regulatory cytokines. These pathways in Allergic Contact Dermatitis ACD are activated by IFN-γ, driven by TNF-α, and as above, apremilast has been shown to block these cytokines in vitro. 