Megakaryocytes from tumor-bearing mice were found to exhibit a pro-inflammatory phenotype displaying increased Ctsg, Lcn2, S100a8, and S100a9 transcripts.141 The functional reprogramming was partly transferred to platelets, equipping them with pro-inflammatory proteins that promote tumor invasion and metastasis.141 Another study showed that hyperglycemia, an established risk factor for tumor metastasis, was shown to alter megakaryocyte metabolism, leading to the production of platelets with increased in vitro adherence to melanoma cells.142. This evidence concerns the gene CTSG and neoplasm.