Smoking and obesity are two leading causes of chronic disease in the developed world. Given that the combined impact of these factors on health can be especially deleterious, it is somewhat ironic that smoking is known to have beneficial effects on body weight; smoking is one of the easiest and most reliable approaches to weight loss, at least for low-level smokers (≤10 cigarettes/day) (1). This phenomenon provides the opportunity to target—and possibly tap into—the mechanisms underlying nicotine’s actions on weight loss. We know, for example, that nicotine stimulates hypothalamic acetylcholine receptors, eventually activating anorexigenic arcuate proopiomelanocortin neurons; melanocortin-4 receptors appear to be crucial to these actions (2). This is particularly interesting because genetic variants affecting the melanocortin system, especially melanocortin-4 receptors, are among the most well-described genetic contributors to human obesity (3,4). The question remains as to how nicotine’s actions on this brain system ultimately affect appetite and metabolism. This is where we pick up the story: extending the mechanisms of nicotine’s actions on weight loss to effectors including brown adipose tissue (BAT) and locomotor activity. In recent years, BAT has become a hot area of study (so to speak) as a result of the discovery of BAT-like tissues …