INTRODUCTION
Sideroblastic anemias (SAs) encompass a group of bone marrow disorders characterized by the abnormal accumulation of iron in the mitochondria of erythroid precursors. This leads to the formation of ring sideroblasts, where iron-laden mitochondria surround the nuclei of erythroblasts 1. Ring sideroblasts can be present in various pathological conditions, including both congenital and acquired forms of sideroblastic anemias 2. The underlying mechanisms leading to different forms of sideroblastic anemias are diverse. However, in all cases, the abnormal accumulation of iron is attributed to disruptions in mitochondrial proteins involved in regulating heme synthesis or Fe/S cluster synthesis. Additionally, impairment in translating mitochondrially encoded proteins contributes to this iron deposition. Consequently, these alterations give rise to ineffective erythropoiesis and iron accumulation in tissues, leading to tissue iron overload 1. It has been associated with antituberculin agents, chloramphenicol, and ethanol. While several etiological factors have been implicated in acquired sideroblastic anemia, including genetic mutations and exposure to toxins3, the association between antiretroviral therapy and the development of Acquired sideroblastic anemia (ASA) is rare and has not been reported to date. Here we report the development of sideroblastic anemia in a patient who was on Dolutegravir therapy. Dolutegravir, an integrase strand transfer inhibitor (INSTI) exerts its antiviral activity by binding to the active site of HIV integrase preventing the stand transfer step crucial in the retroviral DNA integration process thus reducing viral load and slowing down disease progression 4. The association of ASA with Dolutegravir has not been established in the current literature. Naranjo method for estimating the probability of Adverse Drug Reaction (ADR) was used to show the casual association.5