Both IL-32 and Fbxo32 regulate cellular homeostatic control.

We present theoretical aspects of homeostasis loss relevant to disease onset in humans based on identification of candidate target genes and ascertainment of their molecular function. We identify and describe two separate aspects of cellular homeostasis, cell cycle control (IL-32) and redox status (Fbxo32). Remarkably, each of these factors are central transcriptional targets of the NLR family gene and IBD susceptibility factor NOD2. Thus, NOD2 controls two separate aspects of cellular homeostasis, cell cycle control through the senescence modulatory properties of IL32 and cellular redox status through Fbxo32 and involving a recently identified Fbxo32-interacting redox sensor, Nmral2.