To address this, we used a conditional mouse knock‐in model with a heterozygous mutation in the calreticulin gene (Calr+/−), controlled by the Vav1 hematopoietic promoter, which results in persistent thrombocytosis (an increase in circulating platelet numbers) (J. Li et al. 2018). The gene discussed is CALR; the disease is thrombocytosis disease.