Ythdf3, an m6A reader, is involved in crucial biological processes. It has a significant impact on the translation and decay of m6A-modified RNA. By recognizing m6A-modified mRNA, it participates in pathways related to cell metabolism, autophagy, and cancer-related processes, playing an overall important role in maintaining normal cellular functions and in disease development [4].

Ythdf3 has been found to be associated with multiple diseases. In breast cancer, its overexpression promotes brain metastasis by enhancing the translation of m6A-enriched transcripts like ST6GALNAC5, GJA1, and EGFR [1]. In pancreatic cancer, ZDHHC20-mediated S-palmitoylation of Ythdf3 stabilizes MYC mRNA, promoting cancer progression [2]. In autophagy, Ythdf3 is essential for autophagy induction under nutrient deficiency. It promotes autophagy by recognizing m6A modification sites around the stop codon of FOXO3 mRNA and recruiting translation-related factors [3,7]. In liver fibrosis, Ythdf3-mediated PRDX3 translation alleviates the condition [5]. In glioblastoma, it modulates the EGFR/ATK/ERK/p21 signaling axis to promote cancer progression and osimertinib resistance [6]. In melanoma, it regulates metastasis via its target LOXL3 [8]. In castration-resistant prostate cancer, it regulates the degradation and stability of m6A-enriched transcripts to facilitate cancer progression [9].

In conclusion, Ythdf3 is a key player in regulating m6A-modified RNA metabolism, influencing various biological processes and disease conditions. Studies using models like KO/CKO mouse models could potentially further clarify its role in these diseases, providing insights for developing targeted therapies.