Epidermal growth factor receptor (EGFR), a member of the ErbB family, is considered to be overexpressed in gastric cancer and play role in the development of tumourigenesis.9, 10 Recent evidence shows that MICAL‐L1 mediates EGFR endocytosis, overexpression of MICAL‐L1 may lead to the accumulation of EGFR in the late endosomal compartment.11 MICAL‐L2 has been shown to directly implicate in regulating intracellular transport of multiple cell surface receptors and junctional proteins.12, 13, 14 However, whether MICAL‐L2 regulated EGFR endocytosis and recycling pathway remains unclear. The gene discussed is EGFR; the disease is gastric cancer.