Deletion of hspR, which derepresses several chaperones involved in the heat shock response, including ClpB, alpha-crystalin, and DnaK-GrpE-DnaJ1, led to decreased persistence after the initial phase of infection in a mouse model suggesting that dnaK and other HspR regulated genes must be controlled during infection for optimal growth and persistence [19]. The gene discussed is CLPB; the disease is infection.