YTHDF1 knockdown improves the immune paralysis of macrophages, Th1/Th17 cells, and cytotoxic T lymphocytes (CTLs) and also alleviates macrophage-caused endothelial damage in severe sepsis rats with extracorporeal membrane oxygenation (ECMO) by suppressing the high mobility group box-1 (HMGB1)/receptor for advanced glycation end products (RAGE) axis and YTHDF1 and decreasing the m6A RNA methylation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and pJAK2/pSTAT3 proteins in macrophages (53). The gene discussed is JAK2; the disease is Sepsis.