Final answer:
Congenital sideroblastic anemia is typically not due to a defect in Δ-aminolevulinic acid synthase (ALAS); this statement is false. Rather, G6PD deficiency is a common enzyme disorder leading to hemolytic anemia. Thalassemias are different genetic disorders that affect globin chain synthesis.
Step-by-step explanation:
The statement that congenital sideroblastic anemia is most commonly due to a defect in the enzyme Δ-aminolevulinic acid synthase (ALAS) is False. Congenital sideroblastic anemia is typically associated with defects in other enzymes involved in heme synthesis, but not primarily ALAS. In contrast, the enzyme defect most commonly associated with an enzyme deficiency disorder is glucose-6-phosphate-dehydrogenase, or G6PD deficiency, which leads to hemolytic anemia.
For clarity, thalassemias are genetic disorders caused by defects in the synthesis of globin chains. β-thalassemia, for example, arises from a decreased synthesis rate of the β-chain, leading to anemic symptoms due to impaired oxygen transport and shortened lifespan of the red blood cells. α-thalassemia, on the other hand, involves a defect in the α-chain synthesis, but is rarer due to the presence of two gene pairs for the α-chain on the hemoglobin gene.