Another possibility of secondary infection of OSCC as a result of deregulated immune responses is also supported by recent evidence indicating that hyperactivation of IFNγ-induced immunity may cause epithelial destruction with subsequent Candida infection during autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy syndrome, a disease that also correlates with oral cancer development [31]. The gene discussed is IFNG; the disease is candidiasis.