This theory has been partly supported in breast cancer, because a study found that the down-regulation of DSG2 in hypoxic tumours allowed for single tumour cell dissemination, whereas DSG2-expressing tumours generated more CTC clusters; therefore, when considering target treatments, we should try to avoid antibody internalisation and the enhancement of intravasation by deregulating the target molecules [3]. This evidence concerns the gene DSG2 and breast cancer.