To test our hypothesis it is necessary to assess the level of activation of the Src family of non-receptor tyrosine kinases (SFKs), and components of MAPKs cascades in cell cultures obtained from patients affected by Batten disease (JNCL), as well as in the brain cells of mice with different types of deletion in the CLN3 gene [20–22]. This evidence concerns the gene NTRK1 and juvenile neuronal ceroid lipofuscinosis.