The molecular switch or switches that control the activating or inhibitory effect of aPKC on NF-κB in different cell types and the molecular relationship between Par3 and the TNFR pathway will require additional investigations and may have profound implications not only for epithelial response to pro-inflammatory stimuli, but also for diseases involving the aPKC – NF-κB axis such as diabetes and obesity (Sajan et al., 2009a; Sajan et al., 2009b). This evidence concerns the gene PARD3 and obesity due to melanocortin 4 receptor deficiency.