During keratitis, activated inflammatory cells like neutrophil would release series of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1beta (IL-1β),[1] which later induce keratocytes necrosis and collagen degradation in stroma.[2, 3] These activities could result in the thinning of cornea stroma and subsequent scarring formation. This evidence concerns the gene IL1B and keratitis.