In addition to NADK, our efforts revealed potential driver activity for variants of BST1, MAGEA6, ELMOD1, WDR69, THAP10 and IGFBP5. Of these, BST1 and MAGEA6 variants exhibited robust enrichment across multiple screen tumour cores, suggesting that they exhibit potent tumour-driving activity. The gene discussed is BST1; the disease is neoplasm.