They note that SMARCA4 inactivation resulted in greater incorporation of non‐essential SMARCA2 subunits into the SWI/SNF complexes, revealing a role for SMARCA2 in oncogenesis induced by SMARCA4 loss, and they identified that ATPase and bromodomain‐containing SMARCA2 may serve as potential therapeutic targets in these cancers. The gene discussed is SMARCA2; the disease is cancer.