For example, CORO1A inhibited TLR-mediated signal activation in human macrophages55, RAC2 mutations led to different forms of primary immunodeficiencies56, RASAL3 served as a therapeutic target to regulate inflammatory responses in many inflammatory disease states57, ARHGAP30 and ARHGAP9 genetic alterations led to carcinogenesis of colorectal cancer (CRC)58, Vav1 accelerated Ras-driven lung cancer and modulates its tumor microenvironment59,60, and FERMT3 acted as a tumor suppressor gene in GBM and lung cancer61,62. The gene discussed is ARHGAP9; the disease is glioblastoma.