It also increased acetylation of the histones H3 (Lys3) and H4 (Lys8).169 Treatment with panobinostat upregulated cadherin-1 (CDH1) and reversed the M phenotype; CDH1 has been identified as a Wnt-signaling component in invasive breast carcinoma.172 An in vivo study found that salinomycin, a compound that selectively inhibits CSCs,173 in combination with panobinostat, significantly inhibited the growth of TNBC stem cells in TNBC patient-derived xenografts. The gene discussed is CDH1; the disease is invasive breast carcinoma.