To the Editor Dr Shen and colleagues provided a timely and useful Review of the biological links between obesity and cancer. They appropriately identified hepatobiliary cancer as one of the malignancies most strongly associated with excess adiposity and include liver cancer among obesity-related cancers. Yet liver cancer may be harder to accommodate within a broad pan-cancer framework because the pathway from obesity to hepatocarcinogenesis is often mediated less by body size itself than by chronic metabolic liver injury. In the liver, excess adiposity commonly converges with steatosis, inflammatory activity, fibrogenesis, and progressive architectural distortion before hepatocellular carcinoma develops. Thus, the liver is not simply another organ exposed to systemic inflammation, altered hormone signaling, oxidative stress, immune dysregulation, and microbiome changes; it is an organ in which metabolic injury becomes the local carcinogenic milieu. Patients with similar body mass index (BMI) values may therefore have markedly different hepatic cancer risk, and some patients with lower BMI but substantial metabolic dysfunction or fibrosis may be at greater risk than those with higher BMI but less liver disease.