Although many smad-independent pathways in the tumor microenvironment are negatively regulated by the concerted lipid and protein phosphatase activities of PTEN (phosphatase and tensin homologue deleted from chromosome 10) [7], lung cancers, in which mutation of the PTEN gene is rarely observed [8,9], often show hyperactivation of these pathways [9-11]. The gene discussed is PTEN; the disease is neoplasm.