Therefore, our subsequent investigation focused on all CHIP mutations at clonal resolution, revealing that the clonal architecture of MM patients’ CD34+ cells in the apheresis product typically consists of a predominant clone harboring just one variant encompassing 3% to 63% of the cells, along with 1 to 2 minor sub-clones, each representing less than 20% of the cells (Figure 4). The gene discussed is CD34; the disease is Miyoshi myopathy.