in in vitro and transplantation models, which represents a strategy for mitigating hnRNP K-mediated c-Myc activation in patients. Further studies, using fluorescence-anisotropy assays, identified small molecules that specifically disrupt these hnRNP K•MYC interactions. The efficacy of these compounds are now being characterized in vivo. Summary/Conclusion: These findings indicate that increased hnRNP K levels drive c-Myc expression in the absence of MYC translocations or amplifications and that this interaction may be therapeutically targeted.