In this case, IL-17A therapy likely prevented the Th1/Th17 phenotype of psoriasis, skewing the balance to a Th2 immune-associated phenotype feature of eczema, evidenced by the development of generalized eczematous dermatitis.[4] Additionally, and IL-22 and IL17C have crucial roles in the development of eczematous dermatitis.[10]. The gene discussed is IL17C; the disease is atopic eczema.