The study investigates the role of microRNAs in tumor angiogenesis, specifically focusing on the miR-17-92 cluster, which is activated by Myc. Human adenocarcinomas often contain mutations in *KRAS*, *MYC*, and *TP53*, which can promote angiogenesis by increasing vascular endothelial growth factor (VEGF) production. However, Kras-transformed mouse colonocytes lacking p53 formed poorly vascularized tumors, while additional Myc expression promoted robust vascularization and growth. The authors found that Myc-overexpressing tumors had more robust neovascularization, with larger-caliber vessels richly perfused with red blood cells. This effect was not due to increased VEGF production but rather to downregulation of anti-angiogenic thrombospondin-1 (Tsp1) and connective tissue growth factor (CTGF). The miR-17-92 cluster, which is upregulated in colonocytes coexpressing K-Ras and c-Myc, targets Tsp1 and CTGF. Knockdown of miR-17-92 partially restored Tsp1 and CTGF expression, and transduction of Ras-only cells with a miR-17-92-encoding retrovirus reduced Tsp1 and CTGF levels. Notably, miR-17-92-transduced cells formed larger, better-perfused tumors, demonstrating that microRNAs play a crucial role in non-cell-autonomous Myc-induced tumor phenotypes.The study investigates the role of microRNAs in tumor angiogenesis, specifically focusing on the miR-17-92 cluster, which is activated by Myc. Human adenocarcinomas often contain mutations in *KRAS*, *MYC*, and *TP53*, which can promote angiogenesis by increasing vascular endothelial growth factor (VEGF) production. However, Kras-transformed mouse colonocytes lacking p53 formed poorly vascularized tumors, while additional Myc expression promoted robust vascularization and growth. The authors found that Myc-overexpressing tumors had more robust neovascularization, with larger-caliber vessels richly perfused with red blood cells. This effect was not due to increased VEGF production but rather to downregulation of anti-angiogenic thrombospondin-1 (Tsp1) and connective tissue growth factor (CTGF). The miR-17-92 cluster, which is upregulated in colonocytes coexpressing K-Ras and c-Myc, targets Tsp1 and CTGF. Knockdown of miR-17-92 partially restored Tsp1 and CTGF expression, and transduction of Ras-only cells with a miR-17-92-encoding retrovirus reduced Tsp1 and CTGF levels. Notably, miR-17-92-transduced cells formed larger, better-perfused tumors, demonstrating that microRNAs play a crucial role in non-cell-autonomous Myc-induced tumor phenotypes.