SMARCB1 and neoplasm: The dysregulation in the antagonistic interplay between SNF5 (It is encoded by the SAMRCB1) and EZH2 is pivotal in the pathogenesis of tumours propelled by SNF5 inactivation in vivo, the ablation of SNF5 results in heightened expression of EZH2, leading to widespread trimethylation of H3K27, which subsequently represses Polycomb target genes and ultimately contributes to tumorigenesis [61], in specimens from bladder cancer patients, there is a significant downregulation of SNF5 protein expression [24], indicating that SNF5 may impact bladder cancer progression through related pathways.