Several mechanisms have been proposed for the role of Candida albicans in OPMD and OSCC, including the production of nitrosamines, acid aspartyl proteinase, acetaldehyde, and candidalysin (a cytolytic toxin); the overexpression of Ki-67, p53, prostaglandin-endoperoxide synthase 2 (COX -2), and proinflammatory cytokines; the reduction of β-defensins [27]. The gene discussed is MKI67; the disease is oculopharyngeal muscular dystrophy.