SMARCA2 and cancer: This loss of expression is not explained by mutations in the coding sequence of SMARCA2. In an effort to explore the underpinnings of SMARCA2 silencing, we report for the first time that homozygous polymorphisms at the two SMARCA2 promotor polymorphism sites (−741 bp and −1321 bp), previously linked to SMARCA2 silencing in cancer [15,40], do not seem to be a recurrent event responsible for SMARCA2 silencing in SCCOHT.