Cav-1 and Cav-2 conventionally form plasma membrane hetero-oligomers that negatively regulate the activity of several receptors involved in cell proliferation and survival [52]–[54], and therefore their loss is thought to facilitate tumor progression by deliberate activation of different signaling pathways, as observed in the tumor prone Cav-1 knock-out mouse model [55]–[59]. This evidence concerns the gene CAV1 and neoplasm.