As previously outlined, our mathematical modelling of the concept of chronic inflammation in MPNs is also supported by the elegant model described by Hermouet and co-workers [33,35], in which the JAK2 46/1 haplotype was proposed as a marker of inappropriate myelomonocytic response to cytokine stimulation, leading to increased risk of inflammation, myeloid neoplasms, and impaired defense against infection [33]. The gene discussed is JAK2; the disease is infection.