A 7-year-old boy presented to the otolaryngology sleep medicine clinic after being referred by his neurologist for OSA (Video 1). His past medical history was significant for a traumatic brain injury suffered after a dog attack during infancy, resulting in neurologic developmental delay, posttraumatic stress disorder, and attention deficit hyperactivity disorder. He underwent a polysomnogram prior to evaluation, which showed mild OSA with an AHI of 1.7, rapid eye movement (REM) AHI of 6.3, and a low oxygen saturation of 92%. On clinical examination, his tonsils were noted to be a +3 size (75% of oropharyngeal airway) on the Brodsky scale, but there was clinical concern that there may be additional sites of obstruction. He underwent a DISE with T&A one month later, and on postoperative follow-up, his mother did not believe his snoring had improved. A few months later, based on initial DISE findings of a retroflexed epiglottis with lingual tonsil hypertrophy, he underwent an epiglottopexy with lingual tonsillectomy. A postoperative sleep study performed three months after that surgery (and five months after T&A) was concerning for worsening OSA (AHI 4.5; REM AHI 12.1; low O2 saturation 94%). He underwent a second postoperative DISE four months after that polysomnogram, which showed complete collapse of the base of the tongue against the posterior pharynx. When compared to his preoperative DISE prior to T&A, it became apparent that the tonsils were likely not obstructing at the time, but splinting the airway open. The patient was scheduled for a posterior midline glossectomy but was lost to follow-up.