An in vitro study monitoring the protein expression levels of VEGF and its receptor VEGFR2, co-receptor Neuropilin-1, adhesion molecules in TNBC cell lines MDA-MB-231 parental, and metastatic variants to bone and brain MDA-MB-231BO and MDA-MB-231BR in hypoglycemia and hyperglycemia, demonstrated that TNBC progression-related adhesion molecules was linked with overexpression of VEGFR2 in hyperglycemia, while VEGFR2 was sustained and not degraded in hypoglycemia for a rapid switch to its mature functional form upon glucose availability [194]. This evidence concerns the gene VEGFA and Hyperglycemia.