In the field of EGFR TKI-resistant lung cancer, emerging evidence has verified that dysregulated ncRNAs play an indispensable pathophysiological role by modulating crucial signaling pathways such as PI3K/AKT/mTOR, Ras/Raf/MEK/ERK, JAK/STAT and epithelial-mesenchymal transition (EMT) processes to affect resistance to EGFR TKIs [8,10]. This evidence concerns the gene AKT1 and lung cancer.