Two questions relating to the interplay between pericytes and endothelial cells in vivo arise from our work: first, what mechanism underlies the decrease in Desmin-positive pericyte coverage following Egfr signaling inhibition (consequent to inhibitor treatment or genetic ablation of Hb-egf), and second, how does a reduction in pericyte coverage translate into a decreased density of the tumor microvasculature? Here, DES is linked to neoplasm.