Collectively, identification of mutations in a T type Ca(2+) channel (CACNA1G; three families, this study), a voltage-gated K+ channel α subunit (Kv9. 2; KCNS2, 1 family), and voltage-gated sodium channel alpha subunits (SCN4A and SCN11A) in ET families (five total to date) is emerging evidence that problems in regulation of membrane excitability and synaptic transmission, which are important more broadly for motor control and other neuronal network functions, could play a role in the pathophysiology of ET. This evidence concerns the gene KCND3 and essential thrombocythemia.