Cancer patients who receive anticancer treatment develop peripheral neuropathy in up to 60% of cases. Several cytotoxic agents such as epothilones (ixabepilone), platinum compounds (cisplatin, carboplatin, and oxaliplatin), proteasome inhibitors (bortezomib), taxanes (paclitaxel and docetaxel), vinca alkaloids (vincristine and vinblastine), and immunomodulatory drugs (thalidomide) are able to induce a peripheral neuropathy (CIPN). Paclitaxel induces axonal transport disruption via microtubule stabilization, changes in morphology and function of mitochondria, and inflammation. These pathological changes cause symmetrical damage of axons and nerve fiber loss. While a number of reports exist describing the pleiotropic effects of vitamin D and its role in the development of cardiovascular disease, diabetes, and various cancers, less attention has been paid to the effects of vitamin D on the development and function of the nervous system. There is evidence indicating the role of vitamin D in regulating the development and function of nerve cells, The involvement of vitamin D in the function of the central nervous system is supported by the presence of the enzyme 25(OH)D3-1a-hydroxylase, responsible for the formation of the active form of vitamin D, as well as the presence of vitamin D receptors in the brain, mainly in the hypothalamus and dopaminergic neurons of the substantia nigra. The neuroprotective role of vitamin D3 involves the synthesis of proteins binding calcium (Ca2+) ions (e.g., parvoalbumin) and thus maintaining cellular calcium homeostasis, which is very important for brain cell function. Moreover, 1,25-(OH)2D3 administration was shown to down-regulate L-type voltage-sensitive Ca2+ channel expression in rat hippocampal cultures