Sustained mDia2 activation using small molecule intramics (IMMs) reduced U87 and U251 glioblastoma invasion [43], while mDia2 functional inhibition promoted amoeboid motility in a MDA-MB-231 breast cancer model [42, 47], and loss of mDia2 function and/or expression increased single cell dissemination in an ovarian cancer spheroid model [41]. This evidence concerns the gene DIAPH3 and glioblastoma.