KLF17 and neoplasm: For instance, miRNA-145-5p suppresses GC progression by targeting SERPINE1 to inhibit the ERK1/2 pathway,[2] while miR-194-2HG modulates miRNA biogenesis by downregulating BTF3L4, thereby impeding tumor growth.[3] Dysregulated miRNAs, such as miR-409-3p, also influence epithelial-mesenchymal transition and metastasis via KLF17.[4] These findings emphasize miRNAs as central regulators of GC hallmarks, though their causal roles and clinical translation remain underexplored.