However, based on reports of genetic linkage and co-regulation with CYP2A6, coupled with a potential redundancy of function through substrate overlap, it was unclear whether CYP2B6 would influence lung cancer risk independently of CYP2A6. Furthermore, both enzymes are expressed within the lung and localized nitrosamine activation has been linked to nitrosamine-induced lung tumors [2,4,7]. The gene discussed is CYP2A6; the disease is lung carcinoma.