<prompt> Please answer with one of the option in the bracket. Write reasoning in between . Write answer in between .Q:An 18-month-old boy is brought in by his parents for a routine check-up. The parents state that the patient still has not had any language development, and they are concerned about developmental delay. Of note, they have also noticed that the patients facial features have changed significantly in the last year. The patient also seems to have trouble visually focusing on objects or on the television. On exam, the patients temperature is 98.2F 36.8C, blood pressure is 10872 mmHg, pulse is 86min, and respirations are 14min. Of interest, the patient has not increased much in length or weight in the past 3 months. He is now in the 25th percentile for weight but is in the 90th percentile for head circumference. The patient does not appear to have any gross or fine motor deficiencies. Of note, he has coarse facial features that were not previously noted, including a long face, prominent forehead, and protruding eyes. The patient has corneal clouding bilaterally. At rest, the patient keeps his mouth hanging open. After extensive workup, the patient is found to have 2 mutated copies of the IDUA gene, with no production of the protein iduronidase. Which of the following is the likely mutation found in this disease?? A: Chromosomal translocation, B: Interstitial deletion, C: Missense mutation, D: Nonsense mutation, E: Silent mutation,  <response>: This is a clinical vignette describing an 18-month-old boy with developmental delay, coarse facial features, corneal clouding, and open mouth posture. He has macrocephaly and stunted growth. Genetic testing reveals homozygous mutations in the IDUA gene with absent iduronidase protein. The salient features are developmental delay, coarse facies, corneal clouding, short stature, macrocephaly, and IDUA mutations with absent enzyme. This clinical presentation is most consistent with Hunter syndrome, also known as mucopolysaccharidosis type II. It is an X-linked recessive lysosomal storage disease caused by deficiency of iduronidase leading to accumulation of glycosaminoglycans. The IDUA mutations described here are biallelic, indicating they are on both copies of the gene. Biallelic mutations lead to absent protein production, as seen in this patient. The most likely mutation is a nonsense mutation that creates a premature stop codon, leading to no protein production.D: Nonsense mutation 