Brown adipose tissue (BAT) stands out as the sole tissue able to substantially expend energy by leveraging uncoupling protein 1 (UCP1) to increase proton permeability through the inner mitochondrial membrane. The renewed interest in BAT in adult humans resulted from the growing use of 18F-fluoro-deoxyglucose (18FDG) PET coupled with either CT or MRI, and BAT continues to be defined and quantified in vivo according to features visualized through these imaging techniques (1). Inverse associations between the presence of 18FDG-positive adipose tissue and obesity, visceral fat, hyperglycemia, and diagnosis of type 2 diabetes (T2D) have been widely reported (2) and have led to the hypothesis that BAT metabolic dysfunction is a plausible contributor to obesity, T2D, and cardiometabolic diseases. Rodent studies have provided strong support for this hypothesis, as cold-and/or β-adrenergic agonist-stimulated BAT was shown to be a major driver of systemic clearance of glucose and circulating fat. Although BAT is unquestionably considered one of the hottest current targets for the treatment of obesity, T2D, and cardiometabolic complications, we posit that, in contrast to rodents, human BAT is not sufficient to combat cardiometabolic diseases.