We also explored whether the effects of PDIA1 inhibition on cancer–endothelial cell interactions could be attributed to disulphide re-arrangement of integrins known to mediate adhesion of platelets and leukocytes to endothelium [7,26,27,28], to cellular bioenergetics in breast cancer or endothelial cells, an important target for anti-adhesive mechanisms [29], or to alterations in ICAM-1 expression involved in this interaction [30]. This evidence concerns the gene ICAM1 and breast carcinoma.