Our results warrant further investigation into the mechanism found in the xenograft mouse model, as a clear understanding of such a mechanism may facilitate the development of novel therapeutic approaches to suppress ART/NVB-regulated CREB and PGC1α-dependent VEGF expression, thereby controlling tumor growth and angiogenesis through autocrine and paracrine mechanisms (Figure 7). The gene discussed is PPARGC1A; the disease is neoplasm.