Driven by thorough quantitative calibration against time‐course experimental data as well as focused analyses using clinical and pathophysiological data, the models were then used to propose novel mechanistic explanations for the disrupted angiogenic balance in specific human diseases (e.g., suppressed TSP1 expression in tumors due to oncogenic activation of Myc, insufficient induction of VEGF in PAD calf muscle due to dysregulation of microRNA let‐7). This evidence concerns the gene THBS1 and peripheral arterial disease.