CXCR4 and neoplasm of cerebral hemisphere: The results showed that cytokine CXCL12 or supernatant of microglia BV2 cells expressing CXCL12 induced enhanced migratory, invasive and PNI ability of SACC cells in a dose‐dependent fashion, which could be reserved after silencing CXCR4 with siRNA or blocking CXCR4 of SACC cells with AMD3100, which was verified to function as antagonist of CXCR4, thus inhibiting intracranial merisis of primary cerebral tumour.30