Babina et al. reported that (1) prolonged exposure to IL-33 increases the number of mast cells, (2) IL-33 induces swift p38 phosphorylation and stimulates the expression levels of histidine decarboxylase (enhancing histamine synthesis), and (3) IL-33 attenuates degranulation and the expression levels of FcεRI, possibly due to chronic exposure, suggesting an overall stimulating role of IL-33 in ACD pathogenesis with an anti-inflammatory role at the chronic stage (Figure 5) [86]. The gene discussed is IL33; the disease is granular corneal dystrophy type II.