These results have exhibited that (1) NF-κB signaling components play important roles in upregulating more than downregulating m6A-RMRs; (2) JAK/STAT signaling pathways play important roles in upregulating more than downregulating m6A-RMRs except STAT1; and (3) tumor suppressors TP53, PTEN, and APC play significant roles in downregulating more than upregulating m6A-RMRs, suggesting that upregulation of m6A-RMRs may favor more than inhibit tumor progression. This evidence concerns the gene SOAT1 and neoplasm.