In the absence of sufficient chelation therapy, iron excess may escalate to dangerous levels, leading to problems such as organ damage.33 Conversely, beta-thalassemia minor is marked by less severe anemia as it resulting from a singular faulty beta-globin gene.34 Individuals with this illness generally do not necessitate blood transfusions, hence reducing the risk of iron excess from exogenous sources.35 Moreover, the extent of inefficient erythropoiesis is considerably reduced in beta-thalassemia minor, resulting in a better-controlled iron absorption and storage mechanism. The gene discussed is HBB; the disease is anemia (phenotype).