GHR and progeroid syndrome: To analyze genome-wide expression profiles across the extremes of murine lifespan, we compared independent liver microarray datasets from a series of short-lived DNA repair-deficient mouse mutants with severe (Csbm/m;Xpa−/−, Ercc1−/−), intermediate (Ercc1−/Δ−7), mild (Csbm/m) or no significant progeria (Xpa−/−) [7],[9] with mice that show lifespan extension either due to genetic alteration (Ames and Snell dwarf, growth hormone receptor knockout Ghr−/− mice)[20],[21],[22], calorie restriction (CR) [21] or a combination of both (Ames-CR) [21] (Figure 1A).