Studies had demonstrated that THBS1‐CD47 interaction induced endothelial cell apoptosis through disturbing VEGF/VEGFR2 signaling, which was essential for endothelial development.[29] Also, VEGFR2 inhibition was found to promote apoptosis via suppressing STAT3/Bcl‐2 signaling in osteosarcoma.[31] Therefore, we hypothesized if THBS1‐CD47 interaction could medicate mLECs apoptosis via inhibiting STAT3/Bcl‐2 signaling. The gene discussed is BCL2; the disease is osteosarcoma.