Psoriasis vulgaris, a helper T cell TH1/TH17-mediated inflammatory dermatosis, may be effectively treated with biologic medications such as secukinumab, an IL-17A inhibitor. However, suppression of the TH1-mediated axis may result in the paradoxical appearance of TH2-mediated inflammatory skin conditions, such as atopic dermatitis (AD). Dupilumab, a biologic medication that inhibits IL-4/IL-13-cytokines involved in TH2-mediated inflammation-has demonstrated efficacy in treating AD but may result in phenotypic switching to psoriasis. We describe a patient with psoriasis that was well controlled on secukinumab who developed severe AD that improved with dupilumab. After several months of effective treatment with dupilumab, he subsequently developed re-emergence of psoriatic lesions. This case highlights how pharmacologic interventions targeted at specific immunologic pathways, such as the TH1/TH2 axis, may have unintended consequences.