C9orf72 and amyotrophic lateral sclerosis: Current experiments rely on SOD1 transgenic models, which do not recapitulate mitochondrial complex IV deficiency or the genetic heterogeneity of sporadic ALS (such as C9orf72 repeat expansion) and do not assess spinal cord targeting or pharmacokinetic limitations of ferroptosis inhibitors, including low solubility and short half-life.