Since FSP1 is regulated by the NRF2-Keap1 pathway, recent evidence suggests that in cells resistant to ferroptosis due to Keap1 inactivation, like mutant lung cancers, the genetic deletion of NRF2 or FSP1 as well as the pharmacological inhibition of CoQ biosynthesis with 4-chlorobenzoic acid (4-CBA) could represent a novel therapeutic strategy to combat cancer growth [260,261]. The gene discussed is NFE2L2; the disease is lung carcinoma.