Possible explanations include: (1) YTHDF3 is generally considered to act in concert with YTHDF1 and YTHDF2 in m6A regulation, lacking well-defined independent functions; (2) its molecular mechanisms are relatively redundant and difficult to distinguish from its paralogs in immune regulation; and (3) current research has predominantly focused on YTHDF1/2 given their prominent roles in tumor immunity and immunotherapy, leaving the immunological functions of YTHDF3 insufficiently investigated. This evidence concerns the gene YTHDF2 and neoplasm.