Liver fibrosis is a common pathway leading to cirrhosis, which is the final result of injury to the liver.

Debates are inevitable in science and could be a powerful tool for addressing controversial topics as it promotes critical thinking and inspires individuals to consider alternate viewpoints. However, debates can help only to identify the issues that need to be clarified to address this question, but it can never help resolve the controversy itself. In the era of evidence‐based medicine, the need for an evidence‐based debate is mandatory. Polarising opinions and major debate have recently arisen in hepatology on the nomenclature and diagnostic criteria for fatty liver disease associated with metabolic dysfunction (non alcoholic fatty liver disease [NAFLD]‐metabolic (dysfunction) associated fatty liver disease [MAFLD] debate). The aim of this viewpoint is to suggest a way to settle the debate through evidence. Descriptive review using PubMed to identify literature on the evidence and eminence‐based medicine and studies comparing MAFLD and NAFLD criteria. The emerging studies comparing the performance of diagnostic criteria of NAFLD and MAFLD represent the dawn of a new era for reframing the ongoing debate by acquisition of the mandatory evidence that will both resolve the debate and lead to novel avenues of research. In conclusion, the time has come to hold debate and focus on gathering and building the evidence to settle it. It does not matter who wins the debate and once there is robust evidence, we should all follow it wherever it leads.

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Tumor necrosis factor-alpha (TNF-α) is an important cytokine in generating an immune response against infection with hepatitis C virus (HCV). The functions of TNF-α may be altered by single-nucleotide polymorphisms (SNPs) in its gene structure. We hypothesized that SNPs in TNF-α may be important in determining the outcome of an HCV infection. To test this hypothesis, we investigated the role of the polymorphism -308G/A, which is located in the promoter region of the TNF-α gene, in the progression of HCV infection in Egyptian patients using a quantitative real-time polymerase chain reaction (qRT-PCR). The distribution of this polymorphism and its impact on the serum level of TNF-α was compared between 90 HCV-infected patients [45 with HCV-induced cirrhosis and 45 with HCV-related hepatocellular carcinoma (HCC)] and 45 healthy Egyptian volunteers without any history of liver disease. Our results showed that at the TNF-α -308 position, the G/G allele was most common (78.5%) in the study population, with the G/A and A/A alleles occurring less frequently (13.3% and 8.1%, respectively). Frequencies of G/G, G/A, and A/A genotypes were 87%, 7%, and 6% in patients with liver cirrhosis and were 94%, 4%, and 2% in patients with HCC, respectively. Serum levels of TNF-α were significantly higher in HCV-infected patients than in healthy controls, indicating that the TNF-α -308 polymorphism does not influence the production of TNF-α. The serum level of TNF-α was positively correlated with HCV infection. Taken together, these findings suggest that the TNF-α -308 polymorphism may not be a host genetic factor associated with the severity of HCV infection, but may be an independent risk factor for HCC.