Xenografts derived from HBV‐infected HepG2.2.15 cells showed a reduction in BMP9 expression accompanied by an increase in angiogenesis, which was defined based on CD31 staining, and a decrease in pathological vessel normalisation, which was defined based on the expression of a mature vessel marker (α‐SMA) and an immature vessel marker (VEGFR2), compared with HBV‐uninfected HepG2‐derived tumours (Figure 3A,B). Here, ACTA1 is linked to neoplasm.