Recently, research has been carried out on a new potential genetic model of ET, namely on hotfoot17J or Grid2dupE3 mice, which have a genetic mutation of the Grid2 gene (a duplication of exon 3), leading to the mislocalization of the glutamate receptor delta 2 (GluRδ2), and accelerated protein degradation, mimicking the reduced expression of the GluRδ2 protein in the cerebellum of patients with ET [137]. Here, GRID2 is linked to essential thrombocythemia.