The in vitro results revealed a feedforward loop whereby CX3CL1/ICAM-1 signaling in VBMECs stimulated adhesion of NSCLC cells to the microvascular endothelium while the increasing NSCLC cells in turn enhanced the tumor cell-induced CX3CL1 secretion of VBMECs, during which, the invasion of tumor cells was upregulated and the permeability of VBMECs was increased. This evidence concerns the gene ICAM1 and neoplasm.