It is crucial to determine how SWI/SNF complex-mediated chromatin remodeling could modify immune cell function in the tumor microenvironment, to elucidate whether these regulatory mechanisms of SWI/SNF could be exploited to refine the immune checkpoint networks and to identify the context-dependent binding partners of SWI/SNF that could be targeted to achieve durable ICB therapeutic effects. The gene discussed is SMARCA1; the disease is neoplasm.