Introduction Early intervention (EI) may be defined as the set of knowledge-based clinical activities with the intellectually disabled (ID) child and her/his family between birth and approximately six years that intends to eliminate, prevent, or compensate for the developmental delays and deficits of the condition. The strategy is to take advantage of the earlier ages to activate, promote, and optimize neurobehavioral structures and processes which would remain underdeveloped due to adverse neurogenetic effects on the ontogenesis. There are several justifications for carrying out systematic intervention. In the case of a congenital ID condition, assuming early diagnosis, it is advisable to initiate intervention in the weeks following birth in order to reduce as much as possible the delays in the socio-personal, physical, and cognitive aspects of development. Human ontogenesis is highly cumulative. Earlier acquisitions serve as a basis for further developments. The sooner the basic structures are in place, the better the prognosis for additional progress and the higher the probability, assuming continued training, that advanced levels of development as allowed by the condition will be reached. A second reason is that brain plasticity is larger during the first years of life, and this also applies to children with ID therefore supplying a more fertile receptive ground for intervention. The two reasons above suggest that EI is likely to be more cost-effective than any intervention carried on later in life which is not to say that the latter is devoid of value or that intervention with children with ID should be discontinued after six years of age. Guralnick (1997, 2005) has reviewed current knowledge underlying a number of development-enhancing dimensions, concluding that decades of both small- and larger-scale studies indicate that an affirmative answer is warranted to the question whether we are capable of altering individual development through EI programmes. Guralnick (2005) reckons that comprehensive EI programmes have proved able to prevent much of the decline in cognitive development for children with Down syndrome (DS) occurring during the first years. Although demonstrating longer-term effects present difficult methodological challenges, long-term outcomes years later have been documented as well for several developmental pathologies including DS. Guralnick (2005) also suggests directions for future research and practice, among them specifying better subgroups of children and families in research and evaluation studies (etiological and genetic specificity), identifying better the specific components of intervention responsible for producing sought -after effects, calibrating the intensity of intervention, and assessing better patterns of interaction between subgroups based on child's and family characteristics and programme components. But why, it could be asked, should one devoid so much attention to EI and future prospects at a time where, due to the conjunction of fetal diagnosis and abortive practices, the occurrence of babies with DS (and other genetic causes of ID if not today probably tomorrow) is decreasing in a number of Western countries ? Should we not better concentrate our energies on caring for adults with ID who, given the marked increase in their life expectancy, will be more prevalent in coming years than ever in the past? We should certainly pay much attention to this last issue and launch more research and clinical works intending to clarify several of the most urgent problems arising as a consequence of a longer living in persons with ID , such as a propensity towards earlier physiological aging and a higher susceptibility to Alzheimer disease in persons with DS. In my opinion, how ever, the case for EI is far from being closed for reasons that will become apparent in the rest of the paper. Let's take a look at the present-day attempts with animals at genetic therapy in the case of experimentally induced pathological conditions akin to some genetic conditions of ID in humans. …