Metabolic syndrome (MetS) is a complex disorder characterized by the coexistence of phenotypes such as obesity, hypertension, hyperglycemia, high triglyceride level, and low level of high-density lipoprotein cholesterol. Inflammation majorly driven by oxidative stress has an overarching role in obesity and IR-mediated mechanisms leading to MetS. Besides these factors, the molecular linkages between the MetS components and prognostic biomarkers for the prediction of the progression of one component to the others are still elusive. MetS is linked to several morbidities such as type-2 diabetes (T2D), non-alcoholic fatty liver disease, and cardiovascular diseases. Recently, there has been a surge in evidence linking ferroptosis, through iron overload and lipid peroxidation-driven cell death, and diseases such as cardiovascular diseases and T2D. The role of ferroptosis in liver diseases is well characterized as hepatocytes play a major role in iron transport and metabolism. Collectively, the above findings indicate the likelihood of ferroptosis contributing to MetS pathology. Here we have systematically collated and analyzed the high throughput data on MetS generated using various platforms such as GWAS, RNA-seq, and microarrays using a non-quantitative meta-analysis approach to evaluate and compare the expression of molecular mediators of ferroptosis in MetS and its co-morbidities such as T2D and hypercholesterolemia (Fig. 1).