In the nucleus, stable PRMT1 recruited the transcription factor MLXIP, which, in conjunction, bound to the β‐catenin promoter region to form a transcriptional activation complex, significantly enhancing the expression of β‐catenin and its downstream target genes (such as MYC, CCND1, TCF1, etc.), thereby perpetuating the activation of the β‐catenin signaling pathway and ultimately fostering the proliferation, migration, invasion, and in vivo metastasis of GC cells [57]. This evidence concerns the gene PRMT1 and gastric cancer.