Therefore, α3/α5/β4-linked variations could contribute to increased risk of nicotine dependence and to lung cancer, independently and on two levels, (a) by increasing the number of cigarettes smoked and the likelihood of nicotine dependence and (b) by inserting themselves right into the pathophysiologic cascade that leads to lung cancer (Figure 1b). As the authors of the study are careful to point out, reaching a conclusion as to the actual weight of each of these pathways will require studies that take into account other aspects of smoking behavior (for example, age of initiation, puff duration, and depth of inhalation) that may in fact contribute to much of the remaining risk.
