To identify the potential molecular mechanisms by which TFAP2B knockdown inhibited lung cancer cell growth and proliferation, we analyzed the activities of several pro-survival proteins by Western blot and showed that TFAP2B knockdown dramatically suppressed the phosphorylation of ERK1/2 and p38, whereas the levels of total ERK1/2 and p38 protein did not change (Figure 3A). The gene discussed is MAPK3; the disease is lung carcinoma.