Vartak et al. (2017) found that Disarib predominantly binds to the BH1 domain and specifically disrupts the Bcl2-BAK interaction in in vitro biochemical and biophysical analyses (Iyer et al., 2016). Using mouse allograft and xenograft models, the same teams showed that Disarib administration causes tumor regression and exhibits no significant side effects (Vartak et al., 2016). The gene discussed is BCL2; the disease is neoplasm.