Li et al. (2021) reported that in a vincristine (VCR)-induced neuropathic pain (VINP) model, VCR promotes the Ca2+-dependent phosphorylation of calcium/calmodulin-dependent protein kinase II (CaMKII) and activity of the voltage-dependent calcium channel 3.2 subunit (Ca (V)3.2) and that CaMKII and CaV3.2 may activate astrocytes by increasing the level of intracellular free calcium ([Ca2+]i) in the VINP model. These changes promote the Cx43-mediated release of inflammatory factors in spinal astrocytes, leading to the development of NP (Li et al., 2021). This evidence concerns the gene CAMK2G and neuropathic pain.