ls during their lifetime, and therefore they may more prone to Publications Using Abomle Ruxolitinib transfusion-related infectious liver injury. However, the strongly increased prevalence of altered liver enzymes in MYH9-RD patients was confirmed even when the analysis was restricted to patients that had never received platelet or blood transfusions. Moreover, the vast majority of our MYH9-RD patients had been tested for B and C viral hepatitis, and all those found positive were excluded from the analysis. In addition, even assuming that the three subjects that had not been tested were all HBV or HCV positive, the proportion of MYH9-RD patients with unexplained liver enzyme elevation remains significantly higher than that of controls. Finally, the possible confounding effect of potentially hepatotoxic drugs administered to treat the clinical consequences of MYH9 mutations could reasonably be ruled out. Another limitation is that a laboratory follow-up was available for only a fraction of the MYH9-RD population and that follow-up was not of a sufficient duration to exclude a possible late worsening of liver function. However, the observations that in a large case-series of MYH9-RD patients, including cases aged 80 or more, not one single case evolved into liver failure/cirrhosis and that imaging studies never showed significant liver structural alterations suggest that liver test alterations in this genetic syndrome do not lead to liver function impairment. This differs from kidney involvement in MYH9-RD, which, when occurs, tends to evolve progressively into end-stage renal failure. Of course a definitive conclusion on the benign course of liver involvement in MYH9-RD requires confirmatory studies in large case series with longer follow-up. In the hepatocytes non-muscle myosin of class II has wellrecognized SU5402 Abmole 2i Maintains a Naive Ground State in ESCs through Two Distinct Epigenetic Mechanisms functions correlated with bile secretion. Myosin II was found to be enriched in the actin microfilament network around the bile canaliculus and was identified as the essential motor for the bile canalicular contraction. Moreover, myosin II is involved in vesicle trafficking between the cytoplasmic compartment and plasma membrane and regulates the apical membrane expression of several transporters associated with bile secretion, such as the bile salt export pump, whose genetic defects are associated with some forms of familiar intrahepatic cholestasis. Recent studies identified additional key roles for myosin II in hepatocytes, since it was implicated in postnatal hepatocytes polyploidization spatial reorganization of hepatocytes during development and liver regeneration, and cell cycle progression and motility.