Weakly activity of PARP1 caused by LPS or TNFα can help cells response inflammation [22,23,24]; Mild or moderate stresses leads to transcription and DNA repair responses that help to maintain genome stability, in contrast, excessive activity of PARP1 resulted the depletion of NAD+ and accumulation of PAR, leading some metabolic disorder or cell death [4]. This evidence concerns the gene PARP1 and metabolic disease.