In this regard, distinct disease stressors, such as phototoxicity [49], [50], Parkinsonian toxic insults [51], and carcinogens [48], trigger a variety of cell-context-dependent clinical and pathophysiological manifestations upon partial deficits or mutations of Ranbp2. Further, semi-dominant mutations in human RANBP2 cause either acute necrotizing encephalopathies (ANE1) or acute transverse myelitis (ATM) upon exposure to a variety of infectious agents [52]–[54]. The gene discussed is RANBP2; the disease is familial acute necrotizing encephalopathy.