While the potential mechanisms of AFB1 in ESCC risk remain to be elucidated, in an in vitro study, AFG1, a less toxic variant of AFs, is shown to reduce the expression of HLA-I, TAP-1, and LMP-2, critical components in antigen presentation and antigen processing, in adult esophageal epithelial cells, which can ultimately lead to defect in antigen presentation to T-lymphocytes, potentiating tumorigenesis via escaped immune surveillance, therefore potentially linking AF exposure to esophageal cancer [55]. The gene discussed is PSMB9; the disease is esophageal squamous cell carcinoma.