Furthermore, an HA-rich stroma has been shown to facilitate macrophage infiltration and neovascularization, as evidenced by murine models in which exogenous HA enhanced TAM recruitment and vascular remodeling [101] Although direct evidence in HCC is limited, experimental models in glioblastoma and other solid tumors have demonstrated that disruption of HA synthesis or blockade of HA-CD44 interactions reprograms TAMs toward a pro-inflammatory M1 phenotype, thereby restoring antitumor immunity and reducing tumor growth [102]. The gene discussed is CD44; the disease is hepatocellular carcinoma.