Background: Sickle Cell Disease (SCD) is a hereditary chronic haemolytic anaemia with worldwide impact on health and longevity. Sickle cell anaemia (homozygous S gene) is caused by a single missense mutation in the β-globin gene on chromosome 11. At the protein level, sickle haemoglobin arises from a single amino acid substitution (GTG for GAG) at codon 6 of the beta globin gene that results in substitution of valine for glutamic acid. Methods: this research is aimed at determining the relationship between structural variation in the gene for FADS 1 and the severity of sickle cell disease. A total of 50 patients were studied: 25 were severe cases categorized by the criteria listed in the methods section, and 25 non-severe cases who did not exhibit features of severe disease complications. Venous blood (total of 10mls) anticoagulated in ethylene diamine tetraacetic acid (EDTA )and lithium heparin was collected from paediatric and adult sickle cell anaemia patients. The following tests were carried out: full blood count, liver function test, renal function test, DNA extraction and sequencing.