Almost 90 years ago, James Ewing (1866–1943), a physician founder of the American Cancer Society, proposed that heredity is likely to contribute to the etiology of cancer through the indirect transmission of enhanced liability.1 It took us many decades to fully grasp the meaning of this concept, which encompasses not only the primary role of oncogenic genes, but also a much broader set of interacting genetic, environmental and behavioral processes. It is hard to imagine a better example of Ewing's ‘enhance liability factor’ than the case of a single-nucleotide polymorphism working at the crossroads between facilitating behaviors conducive to nicotine dependence and creating a permissive environment for the development of lung cancer. Yet, this is precisely the conclusion we are invited to draw from a recent report2 that illustrates the ability of genome-wide association studies (GWAS) to detect genetic contributions that increase not only the risk of complex bio-behavioral disorders such as addiction, but also the risk of cancer.
