Reexposure to hapten initiates transmigration of the expanded memory T cells to the dermis and epidermis, which interact with antigen-presenting cells followed by the triggering an inflammatory immune response through pro-inflammatory cytokine (TNF-α, IL-1β, IL-6, and IL-23-A) production, resulting in a clinical manifestation of ACD at the sites of hapten challenge [3,4]. This evidence concerns the gene IL6 and granular corneal dystrophy type II.