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. The gene discussed is PTEN; the disease is lung adenocarcinoma.