Inactivation of the p38 pathway promotes cancer development in mice.30–32 Consistent with the tumor-inhibiting effect of p38 on human cancer, we previously reported that the level of activated/phosphorylated p38 (p-p38) was reduced in NSCLC tissue samples compared with normal/normal adjacent lung tissue samples (N/NAT).25 To explore the mechanism responsible for the downregulation of p38 activity in NSCLC, we investigated the relationship between WIP1, a p38 phosphatase overexpressed in cancer, and p-p38. This evidence concerns the gene BRD2 and non-small cell lung carcinoma.