Currently reported and identified mechanisms of drug resistance in lung cancer, not specific to TKI, include increased efflux of drugs due to overly expressed drug transporters, alterations in cell cycle regulatory proteins and/or checkpoints, defects in apoptosis signaling pathways such as anti-apoptotic protein bcl-2 overexpression, and over expression of DNA repair mechanisms (such as nucleotide excision-repair, mismatch-repair, base excision-repair, non-homologous end-joining, and homologous-recombination) [38]–[45]. This evidence concerns the gene PROS1 and lung cancer.