These effects are mediated by increased SWI/SNF chromatin occupancy with ACTL6A expression, as evidenced by Chang et al. (2021), who titrated levels of ACTL6A within the HNSCC cell line FaDu to show that ACTL6A levels are directly tied to SWI/SNF binding at genes necessary for SCC tumor initiation and maintenace23. The gene discussed is ACTL6A; the disease is neoplasm.