The presence of SP in myeloid leukemia cell lines suggests that the undecapeptide could be released from these cells and SP could consequently promote the release of cytokines into the microenvironment of the tumor and the proliferation of tumor cells (by an autocrine/paracrine mechanism), could regulate endothelial cells (expressing the NK-1R) favoring angiogenesis, plasma extravasation and granulocyte infiltration and could activate immune cells expressing the NK-1R (e.g., neutrophils, mast cells); that is, these mechanisms, mediated by SP, amplify the inflammatory response [1,9,102]. This evidence concerns the gene TACR1 and neoplasm.