The upregulated DEGs in breast cancer MSCs included genes related to collagen activation and matrix metalloproteinase (Figure 1C,D), which is indicative of MSC activation in the TME,[24] and genes involved in angiogenesis and immunomodulation, e.g., PDGFRA, PDGFRB, FAP, and THY1, which are critical for tumor progression.[29, 30, 31] These data suggest that MSCs in the TME undergo activation to support tumorigenesis. This evidence concerns the gene PDGFRB and neoplasm.