Further studies supporting the idea of dual inhibition of HH and epigenetic regulators suggest combination therapy of the histone deacetylase inhibitor vorinostat and the SMO inhibitor SANT-1 or the BRD4 inhibitor ZEN-3365 and the GLI1-inhibitor GANT61, both resulting in increased apoptosis and reduced proliferation of AML cells (Hay et al., 2017; Wellbrock et al., 2021) (Figure 2). The gene discussed is GLI1; the disease is acute myeloid leukemia.