There is debate regarding the role of common pathways of tumorigenesis in this disease [25]; for example, previous studies identified RAS mutations, KDR (kinase insert domain receptor, also known as VEGFR2) mutations, MYC gene amplification, and alterations in the p53, CDKN2, NF-κB/IL-6, MAPK, and PIK3CA/AKT/mTOR pathways in angiosarcoma [21,24,45,46,47,48]. This evidence concerns the gene PIK3CA and angiosarcoma.