In this study, we found that SYNGAP1 overexpression obviously suppressed the protein levels of Wnt/β-Catenin signaling key factors including β‐catenin, C-yclin D1 and c-myc in both SW837 and SW1463 cells, suggesting SYNGAP1 may influence READ progression via regulating Wnt/β-Catenin signaling. The gene discussed is SYNGAP1; the disease is reading.