Chemotherapy-induced peripheral neuropathy (CIPN), a dose-limiting neurotoxic effect of chemotherapy, is the most common reason for patients stopping their treatment early thereby increasing the risk of recurrence and decreased survival rate. Inflammatory cascade activation, proinflammatory cytokine upregulation, and neuro-immune communication play essential roles in the initiation and progression of CIPN. Most notably, TNF-α, IL-1β, IL-6, and CCL2 are involved in neuropathic pain experienced by patients undergoing chemotherapy. Further elucidation of the role of these cytokines may lead to their use as biomarkers for predicting the onset of painful peripheral neuropathy and early axonal damage. Evidence is discussed for the involvement of cytokines in CIPN, the possible underlying mechanisms, and their use as potential therapeutic targets to prevent and improve the painful peripheral neuropathy related to chemotherapeutic agents.