The cells responsible for the decline in VEGF-A expression have yet to be identified; however, autocrine VEGF signaling promotes endothelial cell survival [42], and smooth muscle α-actin- (αSMA-) positive cancer-associated fibroblasts (CAFs), which are known to express VEGF-A in the tumor microenvironment [43–45], were less common in tumors from FoxC2+/– mice than in tumors from wild-type mice [15]. This evidence concerns the gene ACTA1 and neoplasm.