The partial suppression of the transcriptional activity of PPAR-γ in heterozygous PPAR-γ-deficient mice results in an improved insulin sensitivity and in a reduced tendency to obesity [41,42] and mice chimeric for wild-type and PPAR-γ null cells exhibit little or no contribution to adipose tissue formation by null cells [43]. The gene discussed is PPARG; the disease is obesity due to melanocortin 4 receptor deficiency.