The authors further showed that supplementation with homocysteine/cystathionine prevented ferroptosis in cysteine‐depleted MYCN‐high adrenergic neuroblastoma cells (which maintain active transsulfuration pathway), but not in cysteine‐depleted MYCN‐high mesenchymal neuroblastoma cells (with inactive transsulfuration pathway), signifying that activated transsulfuration pathway is important for maintaining intracellular cysteine levels for GSH‐mediated protection against ferroptosis. This evidence concerns the gene MYCN and neuroblastoma.