in vitro and in vivo reactivation of the TLR4/MyD88 pathway by LPS in geniposide‐treated HCC did restore the tumour angiogenesis along with an increase of STAT3/Sp1‐dependent VEGF production, suggesting that modulation of STAT3/Sp1 in the TLR4/MyD88 pathway was critical to VEGF‐dependent HCC angiogenesis (Figure 7). The gene discussed is SP1; the disease is neoplasm.