The increase in HIF-1α expression in BM-MSCs in response to breast tumor cells under normoxic conditions is mediated by ROS and JAK/Stat3, and both HIF-1α-dependent and -independent mechanisms increase the expression of VEGF in BM-MSCs to promote the angiogenic sprouting ability of endothelial cells in a VEGF-dependent manner (145). This evidence concerns the gene HIF1A and breast neoplasm.