Obesity is a major, modifiable driver of endometrial carcinogenesis. This review distills how excess adiposity promotes malignant change and synthesizes prevention strategies across the hyperplasia–cancer continuum. Three converging axes underpin risk: aromatase-mediated estrogen excess; insulin resistance with hyperinsulinemia activating PI3K–AKT–mTOR signaling; and adipokine-driven low-grade inflammation with downstream NF-κB/STAT3 activity. Within this framework, EIN is the key precursor in which these pathways coalesce. Risk can be attenuated through progestin-based therapy (levonorgestrel-releasing intrauterine system or continuous oral regimens), structured weight management, and metabolic adjuncts in selected phenotypes (e.g., metformin for insulin resistance; incretin-based anti-obesity agents as emerging options). Bariatric surgery produces substantial weight loss and favorable metabolic shifts, though evidence for cancer risk reduction is largely observational. Overall, a practical precision-prevention approach—combining progestins with durable weight control and metabolic optimization under guideline-concordant surveillance—appears feasible in routine gynecologic care. Future research should establish causal effects, durability, and optimal sequencing/combination of interventions in trials with endometrial endpoints.