Liver cancer, particularly hepatocellular carcinoma (HCC), is a major cause of cancer-related mortality worldwide. Cadmium (Cd), a nonessential toxic metal, has been identified as a significant risk factor due to its widespread presence in industrial emissions, contaminated food, and cigarette smoke. With a long biological half-life, cadmium accumulates in the liver, inducing oxidative stress, DNA damage, and epigenetic modifications, leading to carcinogenesis. The International Agency for Research on Cancer (IARC) classifies cadmium as a Group 1 carcinogen due to its established link with various malignancies, including liver cancer. Cadmium exposure generates reactive oxygen species (ROS), leading to lipid peroxidation, protein oxidation, and DNA damage. It also inhibits DNA repair mechanisms and alters key molecular pathways such as mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/Akt, promoting uncontrolled cell proliferation and inhibiting apoptosis. Hepatocytes absorb cadmium via divalent metal transporter 1 (DMT1) and metallothioneins (MTs), but excessive exposure overwhelms detoxification mechanisms, resulting in hepatocellular injury and fibrosis, which contribute to liver cancer progression. Understanding cadmium’s role in liver carcinogenesis is crucial for developing biomarkers, targeted therapies, and regulatory policies to limit exposure. This review explores cadmium exposure sources, toxicokinetics, and molecular mechanisms in liver cancer, emphasizing the need for further research and public health interventions to mitigate its impact.