A healthy 6-year-old female, vaccinated apart from the seasonal influenza vaccine, presented with 5 days of fever and cough, followed abruptly by worsening mental status and two generalized tonic-clonic seizures. Nasopharyngeal swab was positive for influenza A antigen, amid a severe influenza season.[1] Serum lactate, liver enzymes, platelets, and inflammatory markers were normal. Cerebrospinal fluid revealed 18 WBC/uL, 418 RBC/uL, glucose 70 mg/dL, and protein 144 mg/dL; multiplex meningoencephalitis PCR was negative. MRI showed multiple foci of restricted diffusion and T2 FLAIR hyperintensity in the bilateral thalami, insula, hippocampi, mamillary bodies, brainstem, and cerebellum ([Fig. 1A]). Whole genome sequencing yielded an autosomal dominant, heterozygous RANBP2 pathogenic variant, c.1754 C > T p.(T585M), predisposing to influenza-associated acute necrotizing encephalopathy (ANE).[2] She received oseltamivir, pulse-dose corticosteroids, and supportive care. Her 90-day modified Rankin score was 3 (moderate disability), marked in part by decreased visual acuity (right 20/40, left count fingers at 3 ft), large-angle left sensory exotropia, and bilateral optic pallor ([Fig. 1B]). Optic atrophy was thought secondary to ANE-related intracranial pressure elevation (unmeasured in this case) and/or lateral geniculate nucleus (LGN) injury causing retrograde trans-synaptic optic nerve Wallerian degeneration.[3] Owing to ANE's potential for intracranial hypertension[4] and LGN involvement,[5] [6] survivors should be screened for neuro-ophthalmic complications.