CASP3 and lung cancer: Molecular docking enabled us to demonstrate that the variety of molecules allows the generation of interactions with death receptors that provoke apoptosis by the extrinsic pathway; as well as through the intrinsic pathway by tBID, as generator of the cytochrome C formation, and consequently, the activation of caspase-3, amplifying the apoptotic signal, in addition to showing possible inhibition in EGFR and K-Ras by stopping the growth of lung cancer cells.