It is mainly a combination of factors, including a systemic inflammatory state, increased vascular permeability, endothelial damage, and increased adhesion of tumor cells to each other or the endothelium, caused by the release of pro-inflammatory cytokines such as interleukin 1 beta (IL1B), interleukin 6 (IL6), cathepsin G, interleukin 8 (IL8), and tumor necrosis factor (TNF), as well as increased expression of lymphocyte function-associated antigen 1 (LFA1), intercellular adhesion molecule 2 (ICAM2), and very late antigen 4 (VLA4). Here, ICAM2 is linked to neoplasm.