Collectively, our findings indicate that the cellular context-dependent requirement of BET inhibition cannot be fully explained on the basis of the known molecular functions of BRDs, as also highlighted by largely overlapping gene expression changes in both sensitive and resistant cell lines, or the basal levels of MYC genes, and to date, no genetic, transcriptional or chromatin markers have been identified to predict responsiveness to BET inhibition, except the concurrent mutations in KRAS and LKB1 genes in lung carcinoma models [32]. This evidence concerns the gene KRAS and lung carcinoma.