N⁶-methyladenosine (m⁶A) is the most prevalent posttranscriptional RNA modification in mRNA and long noncoding RNAs of eukaryotes, and its biological functions are mediated by m⁶A writers, erasers and readers. A nuclear methyltransferase complex consisting of METTL3, METTL14, WTAP, VIRMA, ZC3H13, RBM15 (or RBM15B), YWHAG, TRA2A and CAPRIN1 catalyzes the m⁶A modifications, acting as m⁶A writers. m⁶A demethylase ALKBH5 as well as m⁶A demethylase FTO mediate the demethylation of m⁶As, acting as the m⁶A erasers. A variety of proteins including YTH domain-containing proteins can bind m⁶A marks as the m⁶A readers. The role of mRNA m⁶A methylation in COVID-19 patients is of great concern due to reports that m⁶A may provide potential new strategies for the development of vaccine and antiviral drug. For instance, Jun'e et al reported that m⁶A regulators regulate m⁶A during SARS-CoV-2 infection in Huh7 cells. Other studies also show that m⁶A regulators METTL3 and RBM15 are able to regulate host cell innate immune responses during SARS-CoV-2 infection in Caco-2 cells and HuT 78 cells, respectively. Hannah et al found that METTL3 affects SARS-CoV-2 replication in A549 cells, and they found that targeting the m⁶A RNA modification pathway can block SARS-CoV-2 replication. Although many studies have focused on the function and molecular mechanism of m⁶A in cell lines infected with SARS-CoV-2, the clinical relevance and basic molecular characterization of m⁶A in vivo have been neglected, which deserves further exploration.