Aging undermines the efficiency and fidelity of countless cellular processes. While we understand how aging impinges on genomic stability, by compromising cell-cycle checkpoints and DNA repair pathways, and chromatin plasticity, by disturbing physiological nucleosomal density and positioning, its interplay with transcription is less well understood. Though aging has been shown to increase aberrant splicing events, transcriptional errors, and heterogeneity, whether it bears a causal effect in these events and how these erroneous events translate into organismal phenotypes remain to be established.