This results in the inhibition of phosphorylation of Akt, c-Jun, ROCK2, Paxillin, and Cortactin, disrupting focal adhesion maturation and actomyosin contractility, thereby significantly suppressing VM tubular network formation of glioblastoma U-87 MG cells in a dose-dependent manner in vitro (Zhao et al., 2018). The gene discussed is AKT1; the disease is glioblastoma.