ICAM1 and glioblastoma: As the strength of inhibitory interaction determines the licensed NK cells’ potency against encountered target cells lacking the appropriate HLA ligands (17, 21, 68), it is noteworthy that it was higher fractions of KIR2DL1 subsets that expressed LFA-1 and that were in KIR–HLA ligand mismatch with ICAM-1 expressing susceptible GBM cells.