The role of JAK2 mutations in the context of CHIP has been explored by Sano and collaborators, who found that in a murine model of HF, which shows no sign of MPN phenotype, myeloid-directed Jak2VF expression generated circulating mutated myeloid cells, leading to an increase in myocardial inflammation and HF through a signal transducer and activator of transcription (STAT)-1 phosphorylation-dependent mechanism [68]. The gene discussed is JAK2; the disease is hydrops fetalis.