Because these enzymes are essential for the activation of procarcinogens, the susceptibility to carcinogenesis is regulated in part by polymorphisms in the genes that encode these enzymes. A few examples suffice to illustrate this important concept. The product of the P-450 gene, CYP1A1, metabolizes polycyclic aromatic hydrocarbons such as benz(o)pyrene. Approximately 10% of the white population has a highly inducible form of this enzyme that is associated with an increased risk of lung cancer in smokers.^[150] Light smokers with the susceptible genotype CYP1A1 have a sevenfold higher risk of developing lung cancer compared with smokers without the permissive genotype.