Monoamine oxidase B (MAO-B) is a flavin enzyme on the outer mitochondrial membrane that produces hydrogen peroxide during amine deamination and has been implicated as a pro-tumorigenic redox driver in several cancers. Hepatocellular carcinoma (HCC) represents a mechanistic exception: in hepatocytes, MAO-B also catalyzes the oxidation of geranylgeraniol to geranylgeranoic acid (GGA), an acyclic retinoid-like metabolite that, in experimental models, has been shown to eliminate premalignant hepatocyte clones via apoptosis, autophagy, or pyroptosis-like inflammatory cell death. It is hypothesized that the loss of MAO-B expression in aging and chronic liver disease may contribute to a state of relative “GGA insufficiency,” only partially buffered by alternative oxidases, thereby enabling dysplastic hepatocytes to escape elimination and progress to HCC. This perspective reframes MAO-B as a context-dependent metabolic switch and outlines testable implications for biomarker development and chemoprevention in high-risk liver disease.