JAB1 was shown to be increased in the brains of AD patients and APP/PS1 transgenic mice (AD mouse model); JAB1 overexpression strongly increased the RanBP9 protein level by increasing its half-life (Wang et al. 2013); however, whether JAB1 regulates RanBP9 subcellular translocation or its degradation-associated modifications is unknown. Here, RANBP9 is linked to Alzheimer disease.