In fact, we were able to render cells insensitive to Arp2/3 inhibition, just by removing a tumour suppressor gene controlling the G1-S transition, such as RB1 or CDKN1A. There are probably many other ways to escape the control exerted by cortical branched actin and the dissection of the downstream signaling pathway that impinges onto the cell cycle machinery is an important task for future studies. The gene discussed is CDKN1A; the disease is neoplasm.