Deeper dissection of signalling heterogeneity in the context of clinical NSCLC is particularly relevant for KL‐driven tumours: no targeted inhibitors are known for this disease subtype, and LKB1‐mutant NSCLCs have been shown to have an ‘immune‐inert’ state of low programmed death‐ligand 1 (PD‐L1) checkpoint protein 13, 39, 40, making them unsuitable for immunotherapy. This evidence concerns the gene STK11 and neoplasm.