both reported that Efatutazone facilities the treatment of EGFR-TKI-resistant lung adenocarcinoma, by promoting the protein expression of PPAR-γ and phosphatase and tensin homolog (PTEN), causing the inactivation of the Akt pathway without affecting the transcriptional levels, which exerts a synergistic effect with LXRα, a member of another class of nuclear hormonal receptor reported being potential targets for the prevention and treatment of multiple cancers, agonist T0901317 (111, 112). The gene discussed is PTEN; the disease is lung adenocarcinoma.