On the one hand, cell type-specific susceptibility manifests in multiple sclerosis (MS), where oligodendrocytes undergo ferroptosis via the IFN-γ-JAK1/STAT1 axis, reducing SLC7A11 expression that impairs cystine import for glutathione synthesis and leading to myelin basic protein (MBP) peroxidation as cell antioxidant capacity weakens due to decreased glutathione levels, the IFN-γ-JAK1/STAT1 axis activation starts a cascade: IFN-γ binds to receptors, phosphorylating STAT1 through JAK1 activation, which then translocates to the nucleus to regulate ferroptosis-related genes (Lin and Lin, 2010). The gene discussed is STAT1; the disease is multiple sclerosis.