Focusing first on TPO; (a) upregulation of THPO translation, and consequent increased serum TPO levels, resulting from point mutations within the 5ʹ-untranslated region (UTR) that remove upstream AUG codons, is a causative factor in hereditary thrombocytosis [72–76]; whilst (b) point mutations (i.e. R99W [22,71]) and truncations (R31*[68], R157*[71]) within the MPL-binding domain, and frameshift mutations within the C-terminal glycan domain[22] result in reduced levels of serum TPO. Here, MPL is linked to Thrombocytosis.