In the second (elicitation or efferent) phase of the ACD pathogenesis, after re-exposure to the allergen, the allergen-specific memory T cells recognize the foreign substance and activate an inflammatory response mediated by several cytokines (interferon γ (IFN-γ), IL-2 and IL-17), leading to the development of an inflammatory infiltrate responsible for the clinical features of ACD [1]. The gene discussed is IFNG; the disease is granular corneal dystrophy type II.