In contrast to these studies highlighting that increased GLI1 expression contributes to AML pathophysiology, GLI3 expression seems to be actively downregulated in AML patients by epigenetic silencing to not only reduce GLI3R HH repressor function (Chaudhry et al., 2017) but also upregulate the cytarabine chemoresistance-inducing genes SAMHD1, CDA, and MRP8 (Freisleben et al., 2020). Here, GLI1 is linked to acute myeloid leukemia.