Given the upregulated expression of PRMT5 in ACC tumors across all independent datasets used for the analysis (Fig. 2B), its suggested role in suppression of MYC and MYB (the recognized drivers of ACC progression) [45, 96–98], and availability of selective, orally available inhibitors, we focused on evaluating the effect of PRMT5 blockade using in vitro and in vivo models of this rare malignancy. Here, MYC is linked to adrenal cortex carcinoma.