Overexpression or activating mutations in the kinase domain of EGFR increase the kinase activity of EGFR, leading to the hyperactivation of downstream pro-survival genes, and consequently confer oncogenic properties on EGFR, endocytic trafficking and degradation are main EGFR regulator system28, here we found SCEL promotes tumor cell growth via stabilizing EGFR expression in the cells, rather than transcriptional regulation. This evidence concerns the gene EGFR and neoplasm.