It was therefore speculated that SMARCA4 exerts a vital role in genes important for T‐cell differentiation.116 Of particular interest is research suggesting that in contrast to the high incidence of CD8+ lymphomas observed through conditional inactivation of SNF5 (another SWI/SNF‐related complex member),117 the loss of SMARCA4 function did not lead to deregulated cell proliferation and T cell‐derived tumour formation in mutant animals that were over 18 months old. This evidence concerns the gene SMARCA4 and neoplasm.