Our in vitro and in vivo investigations into this mechanism have revealed that the JLSJ prescription effectively impedes Akt phosphorylation, modulates the expression of pro-apoptotic and anti-apoptotic members of the Bcl2 family, induces apoptosis in lung adenocarcinoma cells, and exerts a potent anti-tumor effect. Here, AKT1 is linked to lung adenocarcinoma.