Evidence from another study also suggested that HCC-derived extracellular vehicles (EVs) containing prostate androgen-regulated transcript 1 (PART1), a long non-coding RNA (lncRNA), promoted the M2 polarization of macrophages and enhanced HCC cell proliferation and migration either through the PI3K/AKT or the Janus kinase (JAK)/STAT signaling pathway, suggesting that targeting these EVs may be a potential therapeutic strategy for HCC by inhibiting macrophage polarization and disrupting the tumor-promoting microenvironment [94]. The gene discussed is SOAT1; the disease is hepatocellular carcinoma.