We recently reported that the mutual exclusivity of gain-of-function mutations of EGFR and KRAS, two proto-oncogenes often individually mutated in lung adenocarcinomas (LUADs), can be explained by such synthetic toxicity, despite the fact that products of these two genes operate in overlapping signaling pathways and might have been mutually exclusive because of functional redundancies (Unni et al., 2015). Here, EGFR is linked to lung adenocarcinoma.