In our study, we utilized the AKT-specific inhibitor (MK-2206, 10μM) and activator (SC79, 10μM) to suppress or activate the AKT signaling pathway in lung adenocarcinoma cells with either overexpression or knockdown of SH2D5, in order to investigate whether the effects of SH2D5 could be reversed. This evidence concerns the gene SH2D5 and lung adenocarcinoma.