CRK GENE
It is a co-factor to many Kinases, and sometime act as a regulator
CRK (gene) has been shown to interact with:

• BCAR1,^{[7][8][9][10][11][12][13][14][15]}
• Cbl gene,^[16][17]
• Dock180,^{[18][9][10][19][20]}
• EPS15,^[21]
• Epidermal growth factor receptor,^[22][23]
• Grb2,^{[24][18][25] (A WILD WILD GENE)}
  The focal adhesion kinase (FAK), a protein-tyrosine kinase (PTK), associates with integrin receptors and is activated by cell binding to extracellular matrix proteins, such as fibronectin (FN). FAK autophosphorylation at Tyr-397 promotes Src homology 2 (SH2) domain binding of Src family PTKs, and c-Src phosphorylation of FAK at Tyr-925 creates an SH2 binding site for the Grb2 SH2-SH3 adaptor protein. FN-stimulated Grb2 binding to FAK may facilitate intracellular signaling to targets such as ERK2-mitogen-activated protein kinase. We examined FN-stimulated signaling to ERK2 and found that ERK2 activation was reduced 10-fold in Src- fibroblasts, compared to that of Src- fibroblasts stably reexpressing wild-type c-Src. FN-stimulated FAK phosphotyrosine (P.Tyr) and Grb2 binding to FAK were reduced, whereas the tyrosine phosphorylation of another signaling protein, p130cas, was not detected in the Src- cells.
• IRS4,^[26][27]
• MAP4K1,^[28][29][30]
• MAPK8,^[31]
• NEDD9,^[32][33]
• PDGFRA,^[34][35]
• PDGFRB,^[34]
• PTK2,^[9][12]
• Paxillin^[12][36]
• RAPGEF1,^[37]
• RICS,^[38][39]
• SH3KBP1,^[40] and
• SOS1.^{[25]wikipedia}
•  Crk together with CrkL participates in the Reelin signaling cascade downstream of DAB1.^[2][3]
• ^{We could get your attention that REELIN defect leads to brain MALFORMATION, POINTING TO CRK AND DAB1 AS IMPORTANT TARGET GENES IN SARCOMA!}
•  
  Reelin is a large secreted extracellular matrix glycoprotein that helps regulate processes of neuronal migration and positioning in the developing brain by controlling cell–cell interactions. Besides this important role in early development, reelin continues to work in the adult brain. It modulates synaptic plasticity by enhancing the induction and maintenance of long-term potentiation.^[2][3] It also stimulates dendrite^[4] and dendritic spine^[5] development and regulates the continuing migration of neuroblasts generated in adult neurogenesis sites like subventricular and subgranular zones. It is found not only in the brain, but also in the spinal cord, blood, and other body organs and tissues.
  Reelin has been suggested to be implicated in pathogenesis of several brain diseases. The expression of the protein has been found to be significantly lower in schizophrenia and psychotic bipolar disorder, but the cause of this observation remains uncertain as studies show that psychotropic medication itself affects reelin expression. Moreover, the epigenetic hypothesis aimed at explaining the changed levels^[6] has received some contradictory evidence.^[7][8] Total lack of reelin causes a form of lissencephaly. Reelin may also play a role in Alzheimer's disease, temporal lobe epilepsy and autism.(WIKIPEDIA)
  
   Reelin takes part in the developmental change of NMDA receptor configuration, increasing mobility of NR2B-containing receptors and thus decreasing the time they spend at the synapse.^{[53][dead link][54][55]} It has been hypothesized that this may be a part of the mechanism behind the "NR2B-NR2A switch" that is observed in the brain during its postnatal development.^[56] Ongoing reelin secretion by GABAergic hippocampal neurons is necessary to keep NR2B-containing NMDA receptors at a low level.^[52]
   The Disabled-1 (Dab1) gene encodes a key regulator of Reelin signaling. Reelin is a large glycoprotein secreted by neurons of the developing brain, particularly Cajal-Retzius cells. DAB1 functions downstream of Reln in a signaling pathway that controls cell positioning in the developing brain and during adult neurogenesis