These phenotypic observations were correlated with cellular such molecular changes as disruption of actin filaments, depletion of KRAS, cell division cycle 42 (CDC42), Rac family small GTPase 1 (RAC1), fascin and vinculin and disintegration of vinculin punctates [27,28], suggesting their potential to treat KRAS-mutated cancers. The gene discussed is RAC1; the disease is cancer.