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3. F9 missense mutations impairing factor IX activation are associated with pleiotropic plasma phenotypes

8. DNA base editing corrects common hemophilia A mutations and restores factor VIII expression in in vitroand ex vivomodels

10. 1,3,8-Triazaspiro[4.5]decane Derivatives Inhibit Permeability Transition Pores through a FO-ATP Synthase c Subunit Glu119-Independent Mechanism That Prevents Oligomycin A-Related Side Effects

11. Translational readthrough at F8 nonsense variants in factor VIII B domain contributes to residual expression and lowers inhibitor association

15. Whole-Exome Sequencing in a Family with an Unexplained Tendency for Venous Thromboembolism: Multicomponent Prediction of Low-Frequency Variant Deleteriousness and of Individual Protein Interaction.

17. Translational readthrough at F8 nonsense variants in factor VIII B domain contributes to residual expression and lowers inhibitor association

19. Role of clinical and laboratory parameters for treatment choice in patients with inherited FVII deficiency undergoing surgical procedures: evidence from the STER registry

21. 1,3,8-Triazaspiro[4.5]decane Derivatives Inhibit Permeability Transition Pores through a F O -ATP Synthase c Subunit Glu 119 -Independent Mechanism That Prevents Oligomycin A-Related Side Effects.

23. Not Just Loss-of-Function Variations

34. Additional file 1 of OTC intron 4 variations mediate pathogenic splicing patterns caused by the c.386G>A mutation in humans and spfash mice, and govern susceptibility to RNA-based therapies

35. A naturally occurring mutation in ATP synthase subunit c is associated with increased damage following hypoxia/reoxygenation in STEMI patients

42. Genotype and PK Hemophilia B International Study (GePKHIS) - A progress Report

44. A compensatory U1snRNA partially rescues FAH splicing and protein expression in a splicing-defective mouse model of tyrosinemia type I

46. Circadian rhythms in mouse blood coagulation

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