Kraft et al. 2020 observed that GCH1 overexpression protects cells against ferroptosis triggered by FINs, such as RSL3, IKE, and GPX4. The GCH1-BH4-phospholipid axis controls the endogenous production of BH4, the abundance of CoQ10, and the depletion of unusual phospholipids with two polyunsaturated fatty acyl tails. Soula et al. (2020) demonstrated that tumor cells are sensitive to RSL3, which can directly inactivate GPX4 when GCH1 is deleted or inhibited. This evidence concerns the gene GCH1 and neoplasm.