Further supporting this, CRISPR/Cas9-mediated SMARCA4 knockout in SMARCA4/2-proficient H1437 NSCLC cancer cells conferred resistance to apoptosis induced by cisplatin treatment; knockdown of SMARCA2 in these A4KO cells led to further increased resistance to cisplatin, indicated by reduction of cleaved PARP and cleaved caspase 3 and increased cell viability (Supplementary Fig. 3g, h). This evidence concerns the gene SMARCA4 and non-small cell lung carcinoma.