Background　Chemotherapy-induced neuropathic pain is a common complication in cancer treatment, and is usually intractable because its underlying mechanisms are not clear. G protein gated inwardly rectifying K (GIRK) channels play critical roles in controlling neuronal activity and may be altered in chemotherapy-induced neuropathic pain.　Objective　To review the evidence showing the involvement of GIRK channels in chemotherapy-induced neuropathic pain.　Content　GIRK channels are ubiquitously expressed in neurons, including those in dorsal root ganglion and spinal cord dorsal horn. They are regulated by subunits of G-proteins, 4,5-bisphosphate, protons, etc. GIRK are also coupled with several metabotropic receptors that are importantly implicated in pain signaling, such as, -opioid receptors, B type -butyric amino acid (GABAB) receptors, and 5-hydroxytryptophan receptor 2A, as well. Previous studies revealed that drugs for chemotherapy modulate the levels of protein kinase C, mitogen-activated protein kinase, 5-hydroxytryptamine receptor, and GIRK (i.e. Kir1.1, Kir3.4, and Kir3.1), suggesting the involvement of GIRK in chemotherapy-induced neuropathic pain.　Trend　Further investigation should focus on the effects of drugs for chemotherapy on subtypes of GIRK abundant in neurons in pain signaling pathways, and whether counteracting the effects has potential to relieve intractable chemotherapy-induced neuropathic pain.