Suggests that the prognostic value of Ki-67 on survival was greater in the tumors located in the nodes than that in the primary lesion. Potential limitations of this manuscript include the variation in quantitating Ki-67 staining by immunohistochemistry between the two pathologists. Despite the potential variability of the quantitation of Ki-67 IHC staining, statistical analysis indicated that Ki-67 status was an independent prognostic factor for overall survival and MFS in patients with 1–3 positive nodes. To date, several studies have also indicated that Ki-67 expression may be a marker for predicting the sensitivity of chemotherapy, and that Ki-67 expression before and after neoadjuvant therapy may be employed for predict prognosis. Currently, differences in the Ki-67-detection methods and cutoff points likely contribute to the varied conclusions on the prognostic value of Ki-67 expression in breast cancer patients. Thus, prospective studies with large sample size, standardized methodology and specialized personnel for Ki-67 detection in a single center or international guidelines are warranted. Taken together, Ki-67 expression together with clinical factors may favorably predict the prognosis of breast cancer patients with positive axillary lymph nodes, especially for those with 1–3 positive axillary lymph nodes, which may provide reference for prescribing individualized therapy of breast cancer. Ubiquitination is a key process for the regulation of proteins in the cell and failure of ubiquitin pathways in the brain is linked to neuropathological states such as Parkinson’s disease . The targeting of proteins for ubiquitination relies on enzymes known as E3 ubiquitin ligases and their adaptor proteins; together they identify proteins for the addition of ubiquitin resulting in target protein degradation or alternatively, protein trafficking. Ndfip1 is an adaptor protein for the Nedd4 family of ubiquitin ligases and has been found to be upregulated in neurons after brain injury, including head trauma, stroke and metal toxicity. The upregulation of Ndfip1 is associated with binding and ubiquitination of a number of different protein substrates. One of these is the divalent metal transporter DMT1, which is targeted for ubiquitination and degradation in both the brain and liver in response to rising levels of transition metals. Specifically, Fe2+ and Co2+ can both stimulate increased Ndfip1 levels within primary human neurons in culture. This upregulation leads to a complex forming between Ndfip1, DMT1 and the ubiquitin ligase Nedd4- 2, and results in the ubiquitination of DMT1 followed by its degradation. The removal of DMT1 protects neurons from metal MLN4924 toxicity by limiting metal ion entry. The present study was motivated by studies that report the involvement of DMT1 in the pathogenesis of PD. PD is characterised by the degeneration of dopaminergic neurons in the substantia nigra and the accumulation of cytoplasmic Lewy body inclusions in these neurons. However, PD is also directly associated with the intracellular accumulation of iron, particularly in the substantia nigra.