In contrast, loss of the primary cilia eliminates spatial barriers and results in redistribution of LPAR1 to the plasma membrane, where it binds to Gɑ12 and Gɑq and facilitates the activation of downstream pathways, promoting the proliferative function of LPA and unlocking the potential for unlimited proliferation of GBM cells, consequently maintaining a highly proliferative phenotype. Here, LPAR1 is linked to glioblastoma.