To explore this point in greater detail, we analyzed the function of DUSP5 by in vitro experiment and found that downregulated DUSP5 induced an increase in proliferation and migration of FTC accompanied with overexpression of MMP9 and Vimentin and decreased E‐cadherin protein level, which were molecular markers of migration.28 On the contrary, upregulation of DUSP5 ameliorated the above damaging effect on the tumor growth and metastasis, which obtains preliminary evidence that DUSP5 acts as a key pathogenic factor to mediate the metastasis of FTC, not a biomarker. Here, DUSP5 is linked to neoplasm.