As interferon-alpha2 being a telomerase-inhibitor itself [91], it has been argued that the efficacy of another telomerase-inhibitor-imetelstat which recently has been investigated in ET and myelofibrosis patients [92–94] might actually be mediated through IFN-alpha2 [95] by binding of imetelstat to cell-surface receptors such as toll-like receptor 9 (TLR9) [95] with ensuing TLR9-induced production of type I interferons by plasmacytoid dendritic cells [96]. This evidence concerns the gene TLR9 and essential thrombocythemia.