Interactionswith PGC1-α are reduced in several cancers [21, 185, 186];and oppositely the known CoRs associated with PPARγ are overexpressed and thetranscriptional actions of PPARγ are repressed by epigenetic mechanismsinvolving HDAC3 [187–189].Equally, the control of posttranslational modifications appears to be altered. This evidence concerns the gene PPARG and cancer.