Many downstream targets of Gαo could lead to symptoms of epilepsy or MDs, including inhibiting the expression of adenylyl cyclase, which decreases cyclic cAMP production; N-type (Cav2.2) and P/Q type calcium channel (Cav2.1) activation; and stimulating the opening of inward rectifying potassium channels (1). This evidence concerns the gene CACNA1A and myelodysplastic syndrome.