We thus hypothesize, on the basis of transcriptomic and in vitro data, that the combination between ICAM1 and co-stimulatory molecules such as LFA-1(CD11a/CD18) or ITGAL/ITGB2 could act by activating crucial hub genes in cytotoxic lymphocytes, nature killer cells, TILs and TAMs to promote immune surveillance in the liver cancer microenvironment (Figure 6E). The gene discussed is ICAM1; the disease is liver cancer.