Predicted phase diagrams for SIPA correlates with a variety of hemostasis and thrombosis complications. (A) The platelet agglomeration rate as a function of VWF length and VWF concentration. The filled symbols indicate an agglomeration rate that is above 0.1 with the size of the symbol scaling as the agglomeration rate. The empty symbols correspond to an agglomeration rate below 0.1 , comparable to the level of agglomeration in the absence of sVWF. Plot is in log-log scale. (B) The agglomerate capture rate as a function of VWF length and VWF concentration. The regime with black symbols indicates the capture of an agglomerate. The cross symbols denote the regime showing marginal capture of agglomerate as a transitional SIPA behavior. The white symbols indicate the regime where agglomerates are not captured. (C) The in silico SIPA model should apply to both thrombosis and hemostasis. VWD type 1 or 3 features subnormal concentration or no presence of sVWF, which causes a severe bleeding disorder possibly due to lacking both agglomeration and capture. VWD type 2A/B and acquired VWF syndrome (aVWS), from excessively short VWF lengths, often leads to moderate bleeding possibly due to no capture of agglomerates. The model further predicts NP-VWF can lead to platelet adhesion with marginal capture of agglomerates, which may be required for normal hemostasis. Elevation in sVWF concentration and length leads to a substantial increase of the capture rate (1/capture time) and agglomeration rate, which may be relevant to arterial occlusive thrombosis leading to myocardial infarction (MI) and strokes. The excessive consumption of platelets and consequent bleeding disorders in thrombotic thrombocytopenic purpura (TTP) and thrombotic microangiopathy (TMA) induced by excessive ULVWF may form loose VWF-platelet nets to sequester platelets.