First, we did not perform comparative studies in human macrophages or in murine infection models to evaluate whether activation of the MEK1/2-ERK1/2 pathway was significantly different between non-CF and CF samples; the goal of our study was to evaluate the translational potential of MEK1/2 inhibitor compounds in the context of CF, and not a comparative examination of potential non-CF to CF differences. The gene discussed is MAP2K1; the disease is infection.