Finally, we also propose a mathematical equation that could improve the analysis of animal performance in the inhibitory avoidance task. Neurofibromatosis type 1 is one of the most common autosomal dominant disorders affecting 1 in 3500 individuals world-wide. The clinical diagnostic criteria include cafe´-au-lait spots, dermal or plexiform neurofibromas, Lisch nodules, optic glioma, bony defects and first degree relatives with NF1. In addition to skin pigmentation changes, the hallmark of NF1 is the formation of benign nerve sheath tumors along the peripheral nerves. Neurofibromas are generally small localized tumors that grow near the budding of the nerve. The dermal neurofibromas occur during childhood and grow progressively throughout life, especially during puberty and pregnancy. While these tumors are found in virtually all patients with NF1, there are huge differences in the tumor burden even within family members with the same NF1 mutation. Patients can have anywhere between a few to several thousand tumors. The underlying reason to the differences remains unknown, but it suggests the involvement of epigenetic factors and/or modifier genes. A more complex tumor is found in about one quarter of NF1 patients. The so called plexiform neurofibroma generally occurs before 2 years of age. In contrast to the dermal neurofibromas, pNFA often surrounds the entire nerve, and in some cases can grow extremely large covering entire limbs or large parts of the body. Total excision is often challenging due to their size and location. This is of particular concern as they can undergo malignant transformation and become a malignant peripheral nerve sheath tumor. Patients with NF1 have a 5–13% life time risk of developing an MPNST, often occurring within a preexisting pNFA. Given the difficulties for total excision of a large pNFA and no effective medication, markers that can detect and monitor the progression of pNFA is urgently needed. The MPNST and neurofibroma cells differ from the normal Schwann cell in the expression of receptor tyrosine kinases, making them excellent Gefitinib distributor candidates for drug interventions. The TAM family of receptors has been implicated in a wide range of functions including drug resistance, cell proliferation, cell adhesion and migration. TYRO3 is expressed predominantly within the nervous system, while AXL is ubiquitously expressed. The TAM receptors are activated by a common ligand, GAS6 that has previously been shown to act as a mitogen for Schwann cells. Recent studies showed that GAS6/AXL signaling directs neuronal migration via a signaling pathway involving RAS, RAC, p38MAPK, MAPKAP kinase 2, PI3K and HSP25 resulting in actin reorganization. Up-regulation of AXL mRNA levels was demonstrated in one primary MPNST tumor, but the role of AXL in NF1 tumorigenesis is still unknown. The kinase domain of AXL shares great similarities with the members of the MET tyrosine kinase family. The MET and AXL receptors have been shown to activate similar downstream components. Similar to MET, AXL is commonly up-regulated in drug resistant cell lines and cancers. In addition, MET is often upregulated in NF1 related tumors.