Even if Cav1.2 has never been directly implicated into development of GBS, nor any other neuropathy, we suggest that the recognition of Cav1.2 on a neuron by cross-reacting anti-IVNDT antibodies following ZIKV infection might lead to the initiation of the immune response and development of the GBS pathophysiology (Figure 3). This evidence concerns the gene CACNA1C and Guillain-Barre syndrome.