This observation was corroborated by other studies, which showed that YTHDC2 promoted m6A methylation and subsequently destabilized HOXA13 mRNA to suppress SLC3A2 expression, thereby inducing ferroptosis and inhibiting LUAD tumorigenesis.218 The upregulated reader protein IGF2BP3 recognizes and binds target mRNAs encoding antiferroptotic factors that can undergo METTL3-mediated m6A methylation, leading to suppression of ferroptosis and stimulation of tumorigenesis.219 The writer METTL3 promotes tumor growth and inhibits ferroptosis by stabilizing the m6A modification of SLC7A11 in LUAD.220. This evidence concerns the gene IGF2BP3 and neoplasm.