cancer; obesity; risk

Hepatocellular carcinoma (HCC) is the most common primary cause of liver cancer and is also considered to be the fourth most frequent cause of cancer and the third most common cause of cancer-related deaths worldwide1. The majority of these cases develop due to existing chronic liver conditions such as hepatitis B or C viral infections and alcohol2. However, previous shreds of evidence have shown that 15–50% of HCC is presented as idiopathic and could not be explained with any known etiology3. However, recent studies suggest that nonalcoholic fatty liver disease (NAFLD) can be a possible risk factor for the development of HCC4, and it can act through various mechanisms such as insulin resistance, oxidative stress, steatosis, and imbalances in an interplay of adipokine or cytokine. These are propounded as the most important factors responsible for the pathogenesis and progression of NAFLD that could also have a deterministic role in the pathway of liver cancer as it promotes cell growth and DNA damage. Behavioral therapy and several insulin-sensitizing agents have been tried and tested to achieve a better success rate in the management of this condition5. This approach was alleged as it could help improve insulin resistance and attenuate the necroinflammation, steatosis, and fibrotic changes in the liver parenchyma. Unum castigabis centum emendabis (Rebuke one and correct a hundred). Therefore, an in-depth and detailed understanding of the underlying mechanisms responsible for the mediation of HCC during insulin resistance and identification of its genetic determinants would help in providing actual diagnostic and therapeutic tools of interventions.