Lung cancer is a leading cause of cancer mortality worldwide, 1 and for at least 50 years, primary pathological diagnosis has been based on small biopsies and cytopathological specimens. Until approximately 20 years ago, a simple binary categorisation of small cell and non-small cell lung carcinoma (NSCLC) was, in most cases, sufficient for diagnosis and treatment.However, recent years have seen a rapidly rising proportion of cases of NSCLC amenable to increasingly targeted therapy, initially based on the differential response to systemic treatment of tumours of squamous or glandular differentiation 2 then on the presence of particular mutations in the EGFR gene. [3][4][5] Subsequently, further "driver mutations" have been identified with an increasing percentage having associated treatments. Finally, there is an expanding therapeutic repertoire of immune checkpoint inhibitors with eligibility determined, at least in part, by the expression of immune modulators such as Programmed Death Ligand-1 (PD-L1). 6 In the USA, it is now mandatory to test for EGFR mutations, ALK and ROS1 translocations, and expression of PD-L1. In addition, it is recommended to test for BRAF and MET mutations and RET and NTRK fusions. 7,8 In the UK, for patients with NSCLC of stage IIIB and above, treatments that target genomic abnormalities in EGFR, ALK, ROS1, and quantified expression of PD-L1 are standard-of-care 9 ; those targeting NTRK fusions are approved under certain circumstances 10,11 and those applied to RET and MET abnormalities are currently being assessed by the National Institute for Health and Care Excellence. 12,13 Treatments for a wide variety of other genomic abnormalities are being studied in clinical trials [14][15][16] and adjuvant treatments for