In this issue we highlight a very topical and timely review by Noris and colleagues entitled "New roles for MPV measurement in clinical practice?" [1], and discuss our newly proposed editorial policy for the minimum requirements for future manuscripts that include MPV measurement as their major focus.Fast, precise and reliable measurement of platelet number and size was revolutionized in the 1970s by the widespread availability of automated full blood counters that utilise the aperture impedance or "Coulter" principle that was invented 20 years earlier [2]. As a consequence MPV became an additional parameter of interest to both clinicians and researchers and is routinely available on most modern analysers. One of the fascinating aspects of the normal platelet volume distribution is the classical log-normal distribution demonstrating the heterogeneity of platelet size [3]. This also led to the discovery of the inverse relationship between platelet count and MPV that seems to maintain a remarkably tight control on the total platelet mass between individuals. Having defined normality it soon then became apparent that changes in MPV are associated with both acquired and inherited forms of thrombocytopenia. Noris et al discuss how abnormalities in platelet size using MPV are indeed useful for studying and differentiating between inherited forms of macrothrombocytopenia and giant platelet syndromes from other inherited conditions, and from acquired thrombocytopenias [1,4].However, as they point out, the majority of manuscripts on MPV (1313 papers in Pubmed since 2013; 98 papers which have appeared in this journal since 2006) have focused on the association of MPV with many other clinical conditions such as ischaemic and thrombotic disorders, and their associated clinical outcomes [1]. Many studies have now shown that MPV is raised in patients with thrombosis and can often predict poor outcomes. Norris et al have highlighted a number of important questions. Firstly they question whether a raised MPV is the possible cause of thrombosis or a consequence of the condition, for while there is sound evidence that MPV is influenced by genetic polymorphisms [5], and lifestyle factors [6], these effects account for <20% of natural variation [5,6,7], MPV is also increased following platelet consumption and acceleration of platelet turnover in thrombotic conditions. Noris et al emphasize that the majority of studies were performed during the acute phase of thrombosis which makes these mechanisms highly credible. We would also add that inflammatory mediators, such as IL-6, that are often raised in acute or chronic conditions, may also feedback to the bone marrow, resulting in changes to the whole Megakaryocytic/Platelet axis, polyploidization and consequent thrombopoiesis with a shift towards a more prothrombotic phenotype and a higher MPV [8].Despite these caveats, Noris et al have highlighted a number of population studies that indeed suggest a potential association between MPV and disease. An editorial by Lippi has also recentl...