The Actin-related protein 2/3 complex (ARP2/3) complex has also been implicated in tumor invasion, and a study from our group showed a positive correlation between ARP2/3 overexpression in cancer cells and CRCLM vessel co-option, and that ARP2/3 knockdown resulted in the conversion of CRCLM lesions with a vessel co-option phenotype to angiogenic lesions in vivo14. This evidence concerns the gene ACTR2 and cancer.