IL‐1β derived from alveolar macrophages significantly boosts SAA3 expression, stimulating NF‐κB signaling in a TLR4‐dependent manner in lung ECs and macrophages [99], thereby increasing MMP9 levels in an autocrine manner and creating a conducive lung PMN environment, ultimately promoting pulmonary metastasis of HCC [100]. Here, MMP9 is linked to hepatocellular carcinoma.