In non-small cell lung cancer (NSCLC), oncogene dysregulation due to activating mutations, fusions or amplifications is a frequent event. These recurring oncogenic alterations enable cancer cell survival and growth [1,2]. Lung cancers harbouring oncogenic drivers tend to rely on aberrant signalling for survival and growth, a concept known as ‘oncogene addiction’ [2,3]. This dependency on oncogene signalling, however, generates a unique vulnerability that can be exploited with the use of selective targeted agents such as tyrosine kinase inhibitors (TKIs) [2,4].