ITGAL and liver cancer: 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).