The tumor-host cells interaction underlies these effects in pleural space changes by means of a wide production of molecules, which can be divided, according to their proprieties, in three categories: (1) factors stimulating pleural inflammation (e.g., interleukin 2 - IL2, interleukin 6 – IL6 and TNF); (2) pro-angiogenesis mediators (e.g., angiopoietin 1 and 2 – (ANG-1 and 2); (3) particles promoting vascular hyperpermeability (e.g., VEGF, matrix metalloproteinases—MMP, chemokine (c-c motif) ligand 2—CCL, OPN, etc.)[21]. This evidence concerns the gene ANGPT1 and inflammatory response.