<prompt> Please answer with one of the option in the bracket. Write reasoning in between . Write answer in between .Q:A 4-year-old boy is brought to the emergency department for a right ankle injury sustained during a fall earlier that morning. His parents report that he is clumsy when he runs and has fallen multiple times in the last year. He has reached most of his developmental milestones but did not walk until the age of 17 months. He is an only child and was adopted at age 1. He appears tearful and in mild distress. His temperature is 37.2C 98.9F, pulse is 72min, respirations are 17min, and blood pressure is 8050 mm Hg. His right ankle is mildly swollen with no tenderness over the medial or lateral malleolus; range of motion is full with mild pain. He has marked enlargement of both calves. Patellar and Achilles reflexes are 1 bilaterally. Strength is 45 in the deltoids, knee flexorsextensors, and 55 in the biceps and triceps. Babinski sign is absent. When standing up from a lying position, the patient crawls onto his knees and slowly walks himself up with his hands. Which of the following is the most likely underlying mechanism of this patients condition?? A: SMN1 gene defect, B: Loss of the ATM protein, C: Myotonin protein kinase defect, D: Absence of dystrophin protein, E: Arylsulfatase A deficiency,  <response>: This is a clinical vignette describing a 4-year-old boy with a history of clumsiness, delayed motor milestones, calf hypertrophy, and proximal muscle weakness. The question is asking about the most likely underlying mechanism or diagnosis.Based on the description, the key findings are:- Delayed motor milestones walking at 17 months- Clumsiness and frequent falls - Calf hypertrophy- Proximal muscle weakness deltoids, knee flexorsextensors- Normal reflexes- Difficulty standing up from lying position uses Gowers maneuverThis presentation is most consistent with a muscular dystrophy, specifically Duchenne muscular dystrophy. The calf hypertrophy, proximal weakness, Gowers maneuver, and normal reflexes are classic exam findings. The other answer choices do not fit with the clinical vignette. SMN1 gene defects cause spinal muscular atrophy. Loss of ATM protein leads to ataxia telangiectasia. Myotonin protein kinase defects cause myotonic dystrophy. Arylsulfatase A deficiency causes metachromatic leukodystrophy.D: Absence of dystrophin protein 