The genetic basis of sickle cell anemia lies in a mutation of the HBB gene on chromosome 11, which encodes the beta-globin subunit of hemoglobin. In sickle cell disease, a single nucleotide substitution (adenine to thymine) causes the production of an abnormal form of hemoglobin known as hemoglobin S. This altered hemoglobin shapes red blood cells into a sickle or crescent form, leading to blockages in blood vessels, pain, and complications. The disease is an example of codominance, as individuals with one normal and one mutated gene can have both normal and sickle-shaped cells, providing *malaria* resistance.