There are no reports on the role of epigenetic factors such as DNA methylation and histone acetylation in the pathogenesis of fungal keratitis; however, fungal metabolic products may interact with Toll-like receptors (TLRs), causing a decrease in histone acetylation and an increase in HDAC expression, in a manner similar to that of bacterial infection [34], and then activate downstream NF-κB signaling, leading to the production of inflammatory factors that promote the development of fungal keratitis. This evidence concerns the gene HDAC9 and fungal keratitis.