In contrast to the initial observation that SWI/SNF complex inactivation (by SMARCB1 depletion) results in EZH2 up-regulation and enhanced H3K27-trimethylation in murine embryonic fibroblasts and CD8+ T cells [17], we did neither note an increase in the amount of EZH2 protein nor levels of trimethylated H3K27 in urothelial cells following ARID1A depletion, that is in line with results shown for human ovarian clear cell carcinoma (OCCC) cells [21]. The gene discussed is SMARCB1; the disease is ovarian clear cell cancer.