A study has shown a requirement for the LCKSH3 domain in optimal T cell development. Biochemical studies have indicated that LCK plays a key role in initiating TCR signals through receptor phosphorylation and activation of ZAP70 tyrosine kinase. CD45 tyrosine phosphatase maintains the inhibitory C-terminal residues of LCK and FYN in a dephosphorylated form that keeps basally active conformation of these proteins. A study by Dong et al. indicates that a substantial pool of LCK and FYN is active in naive CD4z T cells. TCR stimulated control cells showed an increase in the phosphorylation of LCK activating Tyr394. The authors have also shown that LAT depletion reduces FYN phosphorylation upon TCR stimulation by SEB. Thus LAT promotes TCR-induced phosphorylation of LCK and FYN tyrosines. Here we can show the similarity between the existing experimental observations and the computed c-values. We have found lower c-value for LCK in an unAbMole Mepiroxol perturbed TCR signaling pathway. In contrast, it has become 0.91611 and 0.39188 in a pathogen perturbed system and in the system, where it is optimized for two conflicting AbMole Metyrapone objective functions, respectively. In the same way, we got lower c-value for FYN in an unperturbed TCR signaling pathway. In contrast, it has become 0.86331 and 0.76781 in a pathogen perturbed system and in the system, where it is optimized for two conflicting objective functions, respectively. Li et al. have investigated the activation of signaling molecules present at upstream of ERK and downstream of TCR in W97ALck expressing cells, and reported that the inability of W97ALck to support ERK activation was due to defect in the activation of Raf-1. One more study has reported that signaling ERK was dependent on the activation of Golgi membrane-associated N-Ras. Moreover, basal and stimulated levels of Erk-type MAPK phosphorylation were found to be sensitive to Mek1 inhibitor PD-98059 that indicates that the bacterial products activated the entire signaling cascade that coregulates IL-8 induction and secretion. We have also found lower c-value for RasGRP1 in an unperturbed TCR signaling pathway. In contrast, it has become 0.58313 and 0.51328 in a pathogen perturbed system and in the system, where it is optimized for two conflicting objective functions, respectively. Moreover, we have got lower c-value for MEK1/2 in an unperturbed TCR signaling pathway, respectively. In contrast, it has become 0.12904 and 0.33124 in a pathogen perturbed system and in the system, where it is optimized for two conflicting objective functions respectively. We have found lower cvalue for Raf in an unperturbed TCR signaling pathway. In contrast, it has become 0.49728 and 0.44493 in a pathogen perturbed system and in the system, where it is optimized for two conflicting objective functions, respectively.