Therefore, abnormal Ca2 + expression and downstream kinase-regulated Tf phosphorylation in AD, especially the regulation of iron homeostasis via tissue-specific phosphorylation of Tf and TfRc, provide new insights into how the CaMKK2-CaMK4 signal affects iron metabolism and highlight mechanisms that require further exploration (Table 1). This evidence concerns the gene CAMKK2 and Alzheimer disease.