However, due to the multi-focal and stochastic nature of this tumor model, in which only approximately 15–20% (based on a total of 400 islets/mouse) of hyperplastic lesions will become “angiogenic” (this frequency is increased by just a few % in Arf−/− mice) the possibility remains that undetected transient alterations in neutrophils in a small subset of lesions could be accounting for the increased incidence of angiogenic switching. This evidence concerns the gene CDKN2A and neoplasm.