The involvement of CYP1A1/CYP1A2 and its inhibition by α-naphthoflavone on ANE-induced events suggest that possibly metabolic activation of ANE components is necessary for some of the ANE-induced carcinogenic events [25] and increase the risk of OSF and oral cancer [57, 58]. Here, CYP1A1 is linked to lip and oral cavity carcinoma.