Interestingly, with the notable differences of thrombocytosis and a lower median age, our patients share with CHIP individuals an unremarkable clinical history, with a very indolent disease, and variants affecting genes regarded as initiator of clonal expansion (e.g., TET2 or ASXL1), as well as genes with higher impact on disease progression (e.g., RUNX1). This evidence concerns the gene RUNX1 and thrombocytosis disease.