In ovarian cancer, MUC16/CA125 overexpression drives oncogenic transformation34 and is associated with poor oncologic outcomes in patients.18,35,36 While MUC16/CA125 is also expressed on healthy ocular surface epithelia, pleural and peritoneal linings, and gynecological tissue,37 its expression has been shown to be entirely dispensable in mice.38 In this context, MUC16/CA125 downregulation in ovarian cancer as a mechanism of resistance to BITEs was unexpected. This evidence concerns the gene MUC16 and ovarian carcinoma.