Finally, the T-type channel CaV3.1-deficiency showed a protective role in EAE (Experimental Autoimmune Encephalomyelitis) mouse model due to reduced cytokine production of granulocyte macrophage colony-stimulating factor (GM-CSF), IL-17A, IL-17F, and IL-21 in Th1 and Th17 cells [197]. Here, CSF2 is linked to experimental autoimmune encephalomyelitis.