In an oxygen–glucose-deprivation model of human SH-SY5Y neuroblastoma cells, HDAC inhibitor treatment led to increased H3K14 and H4K5 acetylation of promoters of brain-derived neurotrophic factor (BDNF), a paracrine neuroprotective factor also implicated in HD, and led to elevated BDNF levels and, consequently, increased viability [40]. The gene discussed is BDNF; the disease is Huntington disease.