To assess whether a permanent increase of circulating platelets may hamper OPC differentiation during remyelination, we used a conditional mouse knock-in model carrying a mutation within the calreticulin gene in a heterozygous fashion controlled by the Vav1 hematopoietic promoter, resulting in sustained thrombocytosis (2–3 times more circulating platelets) without alterations in other cell lineages (Li et al., 2018). The gene discussed is CALR; the disease is Thrombocytosis.