Scientists have been aware for many years of genetic programs that get activated under stress and produce genetic variants in cells that escape nonproliferating conditions. These programs are well conserved in all organisms and expand our view of evolution. They mediate genome instability, create diversity in antibody formation, expand metabolism and increase fitness of pathogens within host environments. Error-prone DNA replication and repair are genetic variability-causing agents that get stimulated by the onset of cellular stresses. Embedded in these programs is the ability to limit mutagenesis to defined genomic regions and times, ensuring integrity of most of the genome. Recent evidence suggests that factors involved in RNA polymerase (RNAP) processivity or transcriptional derepression contribute to the generation of stress-induced mutations. In Bacillus subtilis, transcription-associated mutagenesis has been shown to be independent of recombination-dependent repair and, in some cases, of the Y DNA polymerases. Central to stationary-phase mutagenesis in B. subtilis is the requirement for Mfd, transcription coupling repair factor, which suggests a novel mechanism from those described in other model systems.