MYC and neoplasm: Although the induction of individual target genes by MYC, such as BIM1, contributes to this sensitization (Muthalagu et al., 2014), the aggregate of available data argues that tumor cells that express elevated MYC levels ignore checkpoints that restrict early transcription and that the ensuing trapping of RNAPII is a common mechanism underlying these well-documented vulnerabilities of cells expressing oncogenic levels of MYC, for example by causing conflicts with the replication fork during S-phase that lead to double-strand breaks (Hamperl and Cimprich, 2016).