In the light of these premises and taking into account that: (1) HDAC9 is neurodetrimental in stroke 27; (2) HDACs, including HDAC9, can deacetylate transcription factors on lysine residues 28; (3) TfR1, Fpn1, and Ft expression are up-regulated by HIF-1; and (4) GPX4 transcription is up-regulated by Sp1; the aim of the present work was to determine the role played by HIF-1, Sp1, TfR1 and GPX4 in the signaling of ferroptotic neuronal death mediated by HDAC9 in in vitro and in vivo models of stroke. This evidence concerns the gene HDAC9 and Stroke.