The imposition of MHC restriction on the highly variable TCR has caused heated debate. Two models have been proposed to explain the imposition of MHC restriction. The Germline model proposes that MHC restriction is hard-wired in the TCR Germline sequence due to co-evolution of TCR and MHC to interact with each other. The Selection model suggests that MHC restriction is not a hard-wired property in the Germline sequences of TCRs, but imposed on them by CD4 and CD8 co-receptors during positive selection. The relative importance of the two models are not yet determined. The Germline hypothesis suggests that the ability to bind to MHC is intrinsic and encoded within the germline DNA that are coding for TCRs. This is because of evolutionary pressure selects for TCRs that are capable of binding to MHC and selects against those that are not capable of binding to MHC. Since the emergence of TCR and MHC ~500 million years ago, there is ample opportunity for TCR and MHC to coevolve to recognize each other. Therefore, it is proposed that evolutionary pressure would lead to conserved amino acid sequences at regions of contact with MHCs on TCRs. Evidence from X-ray crystallography has shown comparable binding topologies between various TCR and MHC-peptide complexes. In addition, conserved interactions between TCR and specific MHCs support the hypothesis that MHC restriction is related to the co-evolution of TCR and MHC to some extent. The selection hypothesis argues that instead of being an intrinsic property, MHC restriction is imposed on the T cells during positive thymic selection after random TCRs are produced. According to this model, T cells are capable of recognizing a variety of peptide epitopes independent of MHC molecules before undergoing thymic selection. During thymic selection, only the T cells with affinity to MHC are signaled to survive after the CD4 or CD8 co-receptors also bind to the MHC molecule. This is called positive selection. During positive selection, co-receptors CD4 and CD8 initiate a signaling cascade following MHC binding. This involves the recruitment of Lck, a tyrosine kinase essential for T cell maturation that is associated with the cytoplasmic tail of the CD4 or CD8 co-receptors. Selection model argues that Lck is directed to TCRs by co-receptors CD4 and CD8 when they recognize MHC molecules.