BCAR3 and breast carcinoma: In addition to the phosphorylation-dependent mechanism investigated here, a previous study showed that TGFβ stimulates proteasomal degradation of BCAR3 (Guo et al., 2014), and over-expressed BCAR3 and Cas appear to stabilize each other in breast cancer cells, dependent on their mutual binding (Wallez et al., 2014).