While mutations of Swi3 homologs found in cancer cells are not entirely same as the N-terminal deletion of Swi3 described here in yeast, it might create a similar situation to that of evolved cancer cells, that is, mutations in the SWI/SNF complex associated with an extensive transcriptional reduction and mitigation of the protein burden effect, facilitating rapid growth. The gene discussed is SMARCC1; the disease is cancer.