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Aberrant N6-methyladenosine (m6A) modification of GPX4 mRNA contributes significantly to epigenetic tumorigenesis, and here, we report that selective methyltransferase-like 3 (METTL3)-dependent m6A methylation of GPX4 plays a key role in C5AR1 knockdown-induced ferroptosis induction

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Sang Won Kang and colleagues at Ewha Womans University in Seoul, South Korea, showed that this stress-response enzyme also suppresses the induction of normal programmed cell death mechanisms in a variety of cancer cells