Fig 5-C plots the fractional occupancy of IL-6R on CSCs over time for our baseline level of tumor secretion of IL-6. The model suggests that a fractional occupancy of 12% on CSCs is sufficient to result in the experimentally observed tumor growth rate. In fact, because endothelial cells can secrete higher levels of IL-6 than tumor cells [8], if we were to add endothelial cells to our model then we would expect even greater interdependencies among IL-6, tumor growth dynamics and the tumorigenic potential of CSCs. Here, IL6 is linked to neoplasm.