Studies assessing the pathogenesis of psoriasis subtypes have shown that EP involves significantly higher levels of IL-4 and IL-10, a dramatically lower ratio of Th1/Th2 levels, and a statistically significant difference in T-box expressed in T-cells/GATA-binding protein-3 (GATA-3), as well as IFN-γ/IL-4, when compared to psoriasis vulgaris [3]. In essence, the imbalance in these two cell lines is likely a main driver for EP, where Th1 induces disease, and Th2 promotes inflammation, and the combination of these factors proves advantageous towards the severity of the disease [3]. The gene discussed is GATA3; the disease is psoriasis.