Whole-genome sequencing of 520 esophageal and gastroesophageal junction adenocarcinomas from eight countries found near-identical mutational landscapes in both tumor types, dominated by signatures SBS17a/b, previously tied to acid reflux. These signatures were associated with obesity in esophageal adenocarcinoma. Smoking, a recognized risk factor, left no direct mutational footprint. Signatures reflecting endogenous cellular processes were enriched in high-incidence populations. Beyond the headline, the obesity link carries the most practical weight: it suggests excess body weight may amplify reflux-driven DNA damage rather than act through some separate pathway, fitting the long-standing epidemiological pattern that central adiposity raises reflux and Barrett's esophagus risk. The smoking result is a useful reminder that a risk factor can matter without being mutagenic itself, perhaps by promoting inflammation or cell proliferation. For adults, the message is incremental and reinforcing: weight management and treating chronic reflux remain sensible levers, though this analysis cannot show that losing weight reduces these mutations. The association is cross-sectional and tumor-based, so causality and timing remain unproven, and body-mass data collected across eight countries may be uneven. This is a preprint that has not yet been peer-reviewed, so the signature-to-exposure associations could shift after scrutiny. Overall, this is confirmatory work that sharpens the mechanistic story rather than changing prevention advice.