While the list of indirect mechanisms that can lead to elevated protein steady state levels is extensive, we speculate that the observed increase in RANBP2 protein may be due to either improved chaperone efficiency and/or decreased RANBP2 degradation, given that two heat shock proteins were found to be CA3 binding partners and neurodegenerative disease pathways were found to be down-regulated, which include processes that specifically degrade RANBP2. The gene discussed is RANBP2; the disease is neurodegenerative disease.