Tumors in their development share an array of inflammatory activation mechanisms with leukocytes, including toll-like receptors (TLRs) [32, 75], prostaglandin and leukotrienes' metabolism [76], mitogen-activated protein kinases (MAPKs), that is, extracellular signal-regulated kinases (ERKs), c-Jun NH2-terminal kinases (JNKs) and p38 isoforms (p38s) [77], deregulation of phosphoinositide 3-kinase (PCI3K)/phosphatase and tensin homolog (PTEN)/Akt pathway [78], infiltrating tumor-associated macrophages (TAMs) [31] and lymphocytes T and B [34] and microRNA expression [36]. The gene discussed is PTEN; the disease is neoplasm.