Potential mechanisms underlying ICI efficacy in SMARCA4-UT include (a) high tumor mutation burden [12], (b) enhanced T-cell cytotoxicity due to SWI/SNF complex deficiencies [14], (c) impaired regulatory T cell activation [15], and (d) complex interactions with PD-L1 expression [10][16]. The gene discussed is SMARCA4; the disease is neoplasm.