Herein, we hypothesize that OSM (i.e., which targets EGFR T790M mutation and inhibits activation of AMPK/Lamin-B2/MAPK and PI3K/AKT) in combination with CFM 4.17 NLPFs (i.e., CARP-1 signaling and EGFR activity is inhibited by interacting with EGFR’s ATP binding site) and TLM (i.e., disrupts tumor stromal barriers and leads to enhanced permeation of drugs) will provide superior anti-cancer effects in NSCLC, and by using RNA sequence and the quantitative proteomics, we can identify novel targets that have a role to play in tumor regression. The gene discussed is AKT1; the disease is neoplasm.