Focusing specifically on the four patients with M/LN-Eo and PDGFRA rearrangement, we did not observe any frequent or recurrent cooperating mutations, including in known cancer genes or in genes associated with age-related CH, thus confirming their distinct molecular pathogenesis [17], responsible for a robust and sustained response to tyrosine kinase inhibitors [18]. The gene discussed is PDGFRA; the disease is cancer.