Although data analysis is limited by the small number of FLT3-ITD patient samples with RAS mutations in the Vizome database, we did observe significant enrichment of known C/EBPα targets in RAS mutant AML samples, including ND and innate immune pathways (Supplementary Fig. 16), indicating that RAS mutation-mediated FLT3i resistance may be associated with C/EBPα activation and benefit from combination treatment of guanfacine and FLT3i. This evidence concerns the gene FLT3 and acute myeloid leukemia.