However, the alterations in increased flow velocity in the supplying artery were not accompanied by significant elevations in MVD, VEGF, Ki67, and PCNA, suggesting that the alterations in microcirculation in NAFLD VX2 tumors may be driven by changes in perfusion in the liver itself rather than by angiogenesis or proliferation of the VX2 tumors. This evidence concerns the gene PCNA and metabolic dysfunction-associated steatotic liver disease.