MiR-486-5p is downregulated as a tumor suppressor gene in tumor tissues of lung cancer patients, and overexpression of miR-486-5p disrupts the PI3K/Akt pathway and induces CD133+lung tumor stem cells (CSCs) apoptosis, worthy of happiness is that investigators further demonstrated that treatment with cationic lipid nanoparticles encapsulating miR-486-5p mimic (CCL-486) reduced the percentage of CD133+ and inhibited tumor growth in a xenograft tumor model, which offers a novel technique for novel combination therapy (80). Here, AKT1 is linked to lung carcinoma.