The importance of light and temperature as major factors determining seaweed distribution has been stressed by many authors ; likewise, our field observations and experimental work revealed these factors as being critical for W. setacea survival and growth, and they are probably determining the spread and bathymetric distribution of this species across the Mediterranean Sea. The invasion success of W. setacea in Mediterranean deep water assemblages probably relies on two different abilities. The first one is the ability to maintain permanent carpets all year long, outcompeting both perennial and ephemeral native species. The second ability would be the enhanced and sustained growth of W. setacea, higher than those recorded for other Mediterranean perennial or pseudoperennial native macroalgae growing in deep waters and cultured under the same conditions. Thus, high growth and persistence should be the basis of Womersleyella setacea��s capacity to outcompete native and engineering macroalgae and invertebrates from deep-water Mediterranean bottoms. Additionally, Womersleyella setacea traps sediment and, in this way, it may pre-empt space and prevent the attachment of possible spatial competitors as described for other filamentous species. This makes the settlement of native species and the survival of their juvenile stages impossible, thus reducing the species diversity and equitability of phytobenthic communities. Tumor suppressor PTEN is a dual-specific phosphatase that acts as a negative regulator of the PI3K-AKT-mTOR pathway, thus controlling a variety of processes related to cell survival, proliferation, and growth. PTEN performs a crucial role in the silencing of signal transduction from membrane growth factor receptors through the AKT signaling cascade. Somatic PTEN mutations and deletions or epigenetic silencing are common in multiple tumor types, including breast, endometrium, and thyroid, but also tumors of central nervous system, prostate, lung, melanoma, leukemia and lymphoma. Loss of PTEN can lead to tissue-specific effects, including rapid or slow tumors, or no tumors. In many neoplasms PTEN deletion cooperates with other genetic alternations to enhance tumorigenesis and may determine aggressive clinical behavior of the tumor. Because the AKT pathway dictates multiple downstream processes, including inhibition of apoptosis, tumor-cell proliferation, and DNA repair, and is also known to be associated with radioresistance mechanisms, such as intrinsic radioresistance and hypoxia, inactivation of PTEN may affect the effectiveness of anticancer therapy.