The notion of MDSC encompasses a complex series of cell subsets with the capacity to suppress innate and adaptive immune responses. 1 In 2016, divergences in their immunophenotypic definition led to propose a harmonization/standardization of strategies to establish a robust enumeration of MDSC subsets. Thus, in humans, M-MDSC can be characterized in flow cytometry by the minimal CD14 + /CD11b + /CD33 + /HLA-DR -/low immunophenotypic pattern, at variance from granulocytic MDSC that lack CD14 and express bright CD15. 2 The latter are readily identifiable in mice through the Gr marker but this differentiation antigen is lost on human suppressive neutrophils. These cells can be identified in the low-density fraction of leukocytes after Ficoll Hypaque density centrifugation of human PB, which is a time-consuming technique difficult to standardize. 2 MDSC pertain to the physiological mechanisms allowing to regulate and tamper immune responses. As T-regs or B-regs, they are used by tumour cells to favour their escape from the normally very efficient anti-tumoral immune responses. MDSC are also capable of directly inhibiting T-cell functions. This immunosuppressive action in the setting of malignancy is thought to be due to the secretion by tumour cells and MDSC themselves of various anti-inflammatory cytokines such as TGFβ and IL-10 and many other molecules (arginases, NO, ROS, IDO, PGE2). 3,4 The pejorative role of MDSC in favouring tumour expansion, described in solid tumours, 5 has also been reported in various