The promotion of MDSCs via an IL-6-dependent mechanism can be sustained by the binding of Heat Shock Protein 72 (HSP72), expressed at the surface of tumor-derived EVs, to Toll-Like Receptor 2 on myeloid cells, and the posterior activation of the Myeloid Differentiation primary response 88 (MyD88) pathway, consequently inducing IL-6 secretion and maintaining the MDSC phenotype in an autocrine manner [95]. Here, IL6 is linked to neoplasm.