STK11 and neoplasm: From the cell lines harbouring homozygous SMARCA4-inactivating mutations, we chose NCI-H1819 because it had no detectable wild-type SMARCA4 protein (Fig. 1b) and lacked mutations in other oncogenic drivers or tumour suppressors, including KRAS, EGFR, PIK3CA, BRAF, PTEN, RB1, STK11, TP53 and CDKN2A22, most commonly detected as mutant in NSCLCs, and might therefore produce a phenotype more directly reliant on loss of SMARCA4.