For instance, in MDS, increased inflammation-associated and S100A8/A9-mediated genotoxic stress (Zambetti et al., 2016), ineffective hematopoiesis (Cheng et al., 2019), fatty degeneration with a decline of osteoblastic cells (Krevvata et al., 2014; Wenk et al., 2018), myelofibrosis (Leimkühler et al., 2021), and loss of niche-forming EMCNhi vessels all potentially contribute to the disease. The gene discussed is S100A8; the disease is myelofibrosis.