RNA interference-based loss-of-function assays found that FALEC knockdown inhibited the migration and invasion ability of GC cells through impairing ECM1 expression by exerting its enhancer-like function in cis. Our results not only reveal a novel molecular regulatory mechanism of FALEC in GC, but also indicate a potential biomarker and therapeutic target for individualized treatment of GC patients. The gene discussed is ECM1; the disease is gastric cancer.