Our results demonstrated that LLL12 inhibited STAT3 phosphorylation, expression of STAT3 target genes including Cyclin D1, survivin [19], Bcl-2 [9] and Twist1 [20], and subsequently induced apoptosis as indicated by an increase in levels of cleaved PARP and Caspase-3 in MDA-MB-231, SK-BR-3, and SUM159 breast cancer cell lines (Figure S2). The gene discussed is BCL2; the disease is breast carcinoma.