Many studies on the pathogenesis of GC have demonstrated that the development of GC is the result of combined mutations of multiple genes, like TEAD4‐activated MNX1‐AS1 to promote the progression of GC cells via the EZH2/BTG2 and the miR‐6785‐5p/BCL2 axes.6, 7. Here, BTG2 is linked to gastric cancer.