m6A methylation has been implicated in the pathogenesis of Crohn disease, and YTHDF3, as a key m6A “reader,” participates in the posttranscriptional regulation of inflammation-related genes.[30] In murine models of pneumonia and colitis, elevated YTHDF3 expression has been linked to the suppression of excessive inflammation through the degradation of pro-inflammatory mRNAs.[31,32] In addition to peripheral inflammation, YTHDF3 also plays a critical role in neuroinflammation. Here, YTHDF3 is linked to Crohn disease.