KRAS mutant lung cancers frequently overexpress ACSL3 and thus are equipped to synthesize more MUFA-PLs to protect against ferroptosis (Padanad et al., 2016), while a portion of lung adenocarcinoma cells exhibit high expression of iron-sulfur cluster biosynthesis enzyme cysteine desulfurase (NFS1), thus limiting the reactive iron available for ferroptosis by storing iron in iron-responsive proteins (Alvarez et al., 2017). Here, NFS1 is linked to lung adenocarcinoma.