ECM remodeling and abnormal pro‐metastatic factors expression are crucial in cancer invasion and metastasis.[251, 252] Research indicates that high levels of BACH1 in glioblastomas enhance ECM component expression and accumulation, activate the TGFBR2‐smad2/3 pathway, promote invasive protrusions, induce MMP2 expression and release, and accelerate glioma metastasis.[78, 242] BACH1 fosters the growth and spread of hepatocellular carcinoma (HCC) by upregulating genes related to cell motility, like protein tyrosine kinase 2 (PTK2) and insulin‐like growth factor 1 receptor (IGF1R). This evidence concerns the gene BACH1 and glioma.