In conclusion, LRRC4 is an important tumor suppressor that directly interacts with ERK1/2 to disrupt the MEK1/2-ERK1/2 interaction and anchors ERK1/2 in the cytoplasm to mediate ERK1/2 inactivation, thus blocking ERK-mediated activation of the downstream substrates to suppress cell proliferation and invasion in glioblastoma cells (Fig. 8). Here, LRRC4 is linked to neoplasm.