In practice, the effect of mutations in SMARCA4 in cancer must be interpreted in the context of the status of its paralog SMARCA2. Indeed, in SMARCA4-deficient lung cancer cell lines, knocking down SMARCA2 decreased cell viability, and subsequently restoring different SMARCA4 mutants had varying abilities to compensate for the phenotype caused by SMARCA2 loss [119]. This evidence concerns the gene SMARCA2 and lung carcinoma.