MYC and neoplasm: To examine whether MYC is required for GATAD2B-driven tumor growth in the context of Dox-regulated KRASG12D activation as in Fig. 3d, we used validated shRNA hairpin to knockdown MYC (Supplementary Fig. 8) in the HBEC-iKRAS cells overexpressing GATAD2B. Compared to mice with subcutaneously implanted HBEC-iKRAS cells treated with non-targeting shRNA and maintained on a Dox diet, MYC knockdown significantly decreased tumor formation and eliminated visible metastases (Fig. 5f).