(1) The syneresis of gels formed in wide‐mouthed vessels after the recalcification of oxalate and citrate plasmas is modified by (2) the speed of recalcification, (b) the temperature of the plasma (c) the amount of the surfaces exposed to forces of adhesion.(2) The presence of fat globules and of “blood‐dust” in the before mentioned plasmas does not apparently affect the development of the contraction of clots.(3) The effects of variations of the speed of recalcification and of variations of temperature may be wholly or partly masked when the recalcified gel is formed in small bore tubes.(4) Release of the gel from adhesion to the vessel walls permits syneresis.(5) The development of syneresis in recalcified oxalate and citrate plasmas in contact with flat glass plates is modified by variations in temperature and by other factors at present undetermined.(6) When coagulation is delayed by the anticoagulants named, varying types of syneresis are found. Variations of temperature and the degree of exposure to the forces of adhesion modify the contraction of the clots formed.(7) During the disappearance of platelets after the intravascular injection of “peptone” and of thymus nucleic acid the clots when formed exhibit typical syneresis.(8) Blood platelets are apparently not the primary cause of syneresis.(9) Adhesion plays an important part in the inhibition of syneresis.(10) The absence of platelets may delay the contraction of clots by modifying the viscosity and adhesiveness of blood.(11) The effect of contact on the coagulation of blood is continuous up to the formation of a contracted clot.(12) Attention is drawn to the possible importance of changes of viscosity of the blood in haemorrhagic states.(13) The anomalies apparent by a comparison of the records of various workers on the coagulation and syneresis of normal and of pathological bloods are commented on.The authors are indebted to Dr P. A. Levene for a most generous supply of pure thymus and yeast nucleic acid.