The parallel effects of SMARCB1 and HDACi, in association with an absence of CDKN1C expression in clinical specimens of rhabdoid tumor, and the demonstrated sensitivity of RT cell lines to small changes in CDKN1C expression mediated via siRNA, suggest that loss of CDKN1C is integral to the aetiology of RT, and furthermore that RT may be responsive to specific HDACi that increase endogenous levels of CDKN1C. The gene discussed is SMARCB1; the disease is rhabdoid tumor.