However, the long-term Dex-induced loss of proliferation potential in lung adenocarcinoma cells observed in this study did not occur through canonical senescence pathways involving these proteins such as the p16INK4a/Rb pathway, the p19ARF/p53/p21Cip1 pathway and the PTEN/p27Kip1 pathway, despite the transient early induction of p21Cip1 or the functional linkage between the phenotypic effects of Dex and accumulation of p27Kip1. This evidence concerns the gene CDKN2A and lung adenocarcinoma.