Subjecting them to KRAS ablation/apoptosis, EMT marker analysis, functional assays for tumorigenesis, downstream effector pathways and bioinformatics, we show that modulating their TIMP-1 levels caused alteration in the KRAS -dependency features of NSCLC cell lines affecting apoptosis, EMT marker expression, tumorigenicity, and signaling. The gene discussed is TIMP1; the disease is non-small cell lung carcinoma.