肥胖是子宫内膜癌的已知驱动因素。在本期 JCI 中，Gómez-Banoy 及其同事研究了一组接受免疫检查点抑制剂治疗的晚期子宫内膜癌患者，这些抑制剂针对程序性细胞死亡受体 1 (PD-1) 及其配体 (PD-L1) 之间的相互作用。值得注意的是，体重指数在超重或肥胖范围内与无进展生存率和总生存率的改善存在矛盾的相关性。第二个悖论出现在对内脏脂肪组织的 CT 分析中，内脏脂肪组织在大多数其他情况下被视为不健康的脂肪库，其数量也与治疗结果的改善有关。尽管内脏肥胖作为生物标志物可能具有为个性化治疗策略提供信息的价值，但如果未来鉴定出这种假定的抗癌免疫启动效应的脂肪源性介质，从而产生一种治疗策略，则影响更大。

Obesity is a known driver of endometrial cancer. In this issue of the JCI, Gómez-Banoy and colleagues investigated a cohort of patients with advanced endometrial cancer treated with immune checkpoint inhibitors targeting the interaction between programmed cell death receptor-1 (PD-1) and its ligand (PD-L1). Notably, a BMI in the overweight or obese range was paradoxically associated with improved progression-free and overall survival. A second paradox emerged from CT analyses of visceral adipose tissue, viewed as an unhealthy fat depot in most other contexts, the quantity of which was also associated with improved treatment outcomes. Though visceral adiposity may have value as a biomarker to inform personalized treatment strategies, of even greater impact would be if a therapeutic strategy emerges from the future identification of adipose-derived mediators of this putative anticancer immune-priming effect.