Finally, to demonstrate that enhancement of Elk1 activation by hPIV3-C is completely dependent on ERK1/2 activation, HEK-293T cells were pre-treated with MEK1/2 inhibitor U0126 before stimulation with EGF. This molecule targets MEK1/2 and totally abrogates downstream phosphorylation and activation of ERK1/2 [30] . As shown in Figure 2D , Elk1 activation was blocked by U0126, whereas hPIV3-C expression was maintained ( Figure 2F , right panel). This demonstrates that hPIV3-C is acting through ERK1/2 stimulation. Altogether, these results support a model where hPIV3-C interaction with GRB2 enhances cellular response to growth factors as assessed by an increased activation of MAPK/ ERK pathway.