1. IntroductionThe thalassaemias are a group of inherited haematological disorders caused by defects in the synthesis of one or more of the globin chains. It is an autosomal recessive disorder and affects men and women equally. Approximately 5% of the world’s population has a globin variant, but only 1.7% has alpha or beta thalassaemia trait [1]. α-thalassaemia and β-thalassaemia is caused by reduced or absent synthesis of α and β globin chains respectively [2].Globally, the most common single gene disorders of haemoglobinopathies are haemoglobin E (HbE) and sickle cell anaemia (HbS) [3]. The primary feature of this illness is decreased or non-existent production of either the β-like or the α-like globin chains to form haemoglobin tetramers during foetal and postnatal life [4].The α/β thalassaemia and hereditary persistence of foetal haemoglobin (HPFH) are the disorders of haematopoiesis, caused by large deletions in both α and β globin genes and show raised foetal haemoglobin (HbF) levels in adult life [5]. With both types of thalassaemia occurring at such high frequencies, and the fact that α and β-globin genes are inherited on 2 different chromosomes (the α-globin gene on chromosome 16 and β-globin gene on chromosome 11), it is not uncommon for individuals to inherit α-thalassaemia trait from one parent and β-thalassaemia trait from the other. It is well known that the diagnosis of double heterozygotes of α and β-thalassaemia poses challenges both during diagnosis and treatment. This has been documented since 1982 [6-8] and summarised in Weatherall and Clegg [9]. Although, it is not documented, the frequency of α/β thalassaemia in Bangladesh is being detected more in the recent years. In this case, a 4 month old patient is diagnosed with α/β thalassaemia with the help of genetic testing.