Chalmin et al describe that heat shock protein 72 (HSP72) expressing exosomes derived from different solid tumor cell lines, account for MDSC activation through triggering of STAT3 in a Toll-like receptor 2 (TLR2)/myeloid differentiation protein 88 (MyD88)-dependent manner through an autocrine IL-6 production, whereas tumor-derived soluble factors are responsible for MDSC expansion [102]. This evidence concerns the gene STAT3 and neoplasm.