In a recent publication in Cancer Cell, Jana et al. uncover a phenomenon they call ‘transcriptional-translational conflict’ (TTC) where deletion of the ARID1A tumor suppressor elevated proliferation-associated transcripts, but up to 70% of upregulated mRNAs displayed no corresponding change in protein levels.1 The clinical implication of these findings is that patients with ARID1A-deficient bladder tumors may be susceptible to treatment with pharmacological inhibitors of protein synthesis. The gene discussed is ARID1A; the disease is cancer.