The stress response is an evolutionarily, highly conserved adaptive mechanism that enhances cell survival. Genome instability is a hallmark of cancer cells. We are highly interested in the relationship between these two factors. We use mouse models to mimic lung cancer, which have obvious genome instability. We also use molecular methods to find the basis for how these pathways talk to each other. This work might give us some clue or target for new pharmaceutical approaches based on protein stress.