Overexpression of Sall2 inhibits DNA synthesis and increases apoptosis of ovarian cancer cells, effects accompanied by increased expression of p21WAF1 and BAX proteins.12 Consistently, Sall2 was found to directly regulate the proapoptotic BAX after treatment of human ovarian surface epithelial (HOSE) cells with etoposide.20 In addition, treatment of HOSE cells with etoposide slightly increases both Sall2 levels and Sall2 binding to the c-Myc promoter.21 The latter was associated with c-Myc repression and cellular apoptosis. The gene discussed is SALL2; the disease is ovarian carcinoma.