Belgium is investigating alternatives for the treatment of infections with multidrug resistant infectious agents, like phage therapy. In this regard, telomere shortening occurs associated to mouse and human aging and has been proposed to be rate-limiting for organismal life span. Importantly, telomere shortening associated with aging is observed both at stem cell and differentiated compartments in humans and mice , opening the possibility that telomere erosion with age may be responsible, at least in part, for the decline in stem cell functionality associated to the aging process. This notion is supported by telomerase-deficient mice with short telomeres, which show severely compromised epidermal stem cell functionality with increasing mouse generations. Likewise, severe telomere attrition in these mice leads to the occurrence of a dwarf phenotype. The tumor suppressor protein p53 is activated and mediates the cellular response to various types of DNA damage, including telomere dysfunction. In particular, abrogation of p53 rescues male germ cell depletion in telomerase-deficient mice with short telomeres, suggesting that p53 senses telomere damage in stem/progenitor cell populations and leads to massive germ cell apoptosis. In turn, p53 abrogation also impairs the tumor suppressor activity of short telomeres leading to increased tumorigenesis in telomerase deficient mice simultaneously lacking p53. Most cancer cells display some type of chromosomal rearrangement. Whereas solid tumors usually display complex karyotypes with many different types of chromosomal rearrangements, many hematological malignancies and certain sarcomas display only one or a few aberrations, usually balanced chromosomal translocations, which in some cases have been shown to be the initiating event in tumor development. We also suggest that growth factors starvation prior to NPC transplantation might enhance the ability of these cells to graft and provide functional recovery. The observations concerning the organized sprouting of astrocytes and BAY-60-7550 439083-90-6 neurons after growth factors withdrawal could result in a better targeting of the transplanted cells to the lesion site. Rather than providing optimal surviving conditions for cultures, we hypothesize that adjusting culture parameters might be essential for achieving success when grafting these cells in damaged systems. Similar to ischemic cell conditioning where pre-exposure of neural cells to brief ischemic episodes render these cells rather resistant to subsequent ischemia , it is possible that transitory withdrawal of EGF and FGF-2 might trigger the expression of specific gene programs for differentiation and/or neuroprotection. The differences found in neuronal and glial differentiation between the CTR and MFM groups, give rise to a new question: Can growth factors removal influence the capability of migration, integration and differentiation of NPC after cell transplantation? This is an important issue to be evaluated and could be relevant for the functional recovery of neurological disorders.