Hemochromatosis is a metabolic disease that causes iron accumulation in the body. It is described by excessive iron levels in the blood, skin, joints, and internal organs, such as the liver, pancreas, pituitary glands, and even the heart, thus referred to as a systemic inflammatory condition that might be due to genetic or unknown etiology. Though hereditary factors are a primary reason for this condition, inflammation-mediated hemochromatosis occurs in chronic metabolic dysfunction, particularly with overexpression of hepcidin. The relationship between reactive oxygen species (ROS) and inflammation-mediated hemochromatosis is a self-perpetuating pathological mechanism, where iron sequestration and inflammatory conditions synergistically affect the production of ROS and are directly related to oxidative stress and lipid peroxidation. Subsequently, ferroptosis, an iron-dependent cell death, is unique from all the other apoptosis and closely related to lipid and iron metabolism. The interlink between ROS and ferroptosis plays an indispensable role in inflammation, which has an impact on the pathophysiology of inflammatory hemochromatosis. Understanding this triad of ferroptosis-ROS-inflammation impact could provide novel insights into redox biology and therapeutic advancements.