In MM, both JAK1 and JAK2 presented overexpression in a proportion of patients, and Ruxolitinib treatment in combination with Bortezomib, Itacitinib or Daratumumab inhibited JAK/STAT3 phosphorylation, upregulated CD38 expression, inhibited in vitro and in vivo myeloma cell growth and induced cell apoptosis and subG0 arrest [73,143,144]. The gene discussed is JAK1; the disease is Miyoshi myopathy.