Our previous work has reported that MICAL2 is the major regulator of breast cancer cell migration through inhibiting EGFR/P38 signalling activation.24 In the current study, we further extended our observation on MICAL‐L2 that lacks flavoprotein monooxygenase (MO) domain and owns C‐terminal domains (CTD) compared with MICAL2.25 We showed that gastric cancer cell migrative potential was greatly impaired, which was likely mediated by the knockdown of MICAL‐L2 expression, whereas overexpression of MICAL‐L2 increased cell motility. The gene discussed is EGFR; the disease is gastric cancer.