11β‐Hydroxysteroid dehydrogenase type 1 (11β‐HSD1) catalyses the intracellular conversion of inert cortisone to physiologically active cortisol, functioning to enhance local cortisol action beyond what would be predicted based on simple plasma exposures. Adipose tissue overexpression of 11β‐HSD1 in rodents to levels observed in human obesity can lead to a near complete metabolic syndrome phenotype, and inhibition of 11β‐HSD1 has been proposed to be of potential therapeutic benefit to patients with type 2 diabetes mellitus (T2DM). Recently published clinical results with the selective 11β‐HSD1 inhibitor, INCB13739, have, for the first time, provided evidence substantiating this hypothesis, and suggest that 11β‐HSD1 activity may be important in regulating glycaemia and cardiometabolic risk. In patients with T2DM failing metformin monotherapy, INCB13739 treatment achieves significant reductions in haemoglobin A1c (HbA1c) and fasting plasma glucose (FPG), and when present improves hyperlipidaemia and hypertriglyceridaemia. Interestingly, these positive effects are observed primarily in subjects categorized as obese (body mass index, BMI > 30 kg/m²) and not in subjects categorized as overweight (BMI ≤ 30 kg/m²), underscoring the likely importance of adipose tissue 11β‐HSD1 activity to the cardiometabolic sequelae of obesity. This review summarizes the therapeutic rationale for 11β‐HSD1 inhibition, and describes in detail the metabolic and endocrinologic changes observed in patients with T2DM treated with INCB13739.