Background and Objectives: Metabolic and bariatric surgery improves obesity and metabolic dys-function-associated steatotic liver disease (MASLD), but its effect on the residual risk of hepatocellu- lar carcinoma (HCC) is less clearly defined. This narrative review examines the relationship between postoperative metabolic improvement, fibrosis regression, and HCC risk, with particular attention to surveillance. Materials and Methods: A targeted literature search identified clinical studies, mechanistic investigations, and professional guidance relevant to bariatric surgery, MASLD, and HCC. Results: Randomized and paired-biopsy studies support improvement in steatohepatitis, whereas observational cohorts associate surgery with lower HCC occurrence and fewer major adverse liver outcomes. These findings address different endpoints and should not be treated as interchangeable evidence of cancer prevention. Advanced fibrosis can persist despite substantial weight loss and resolution of steatohepatitis. Conversely, the absolute postoperative HCC risk among patients with documented fibrosis regression remains insufficiently characterized. The available evidence does not establish a postoperative biochemical, elastographic, or histological threshold at which surveillance can safely be stopped in patients with established cirrhosis. Conclusion: Surveillance decisions should therefore remain anchored to the underlying liver disease, treatment eligibility, and applicable guidance rather than weight loss alone. Noncirrhotic advanced fibrosis requires individualized assessment because professional recommendations differ and evidence is limited. Future studies should report HCC separately from composite liver outcomes and evaluate risk according to baseline and postoperative fibrosis, metabolic trajectories, and surveillance exposure. Bariatric surgery may modify the course of liver disease, but metabolic improvement should not be equated with elimination of carcinogenic risk.