The V617F substitution induces a conformational shift that alleviates repressive interactions between its JH1 and JH2 domains, resulting in the constitutive activation of JAK2 (22,23), which enhances downstream signaling pathways, such as Janus kinase (JAK)-signal transducers and activators of transcription (STAT) and leads to the proliferation of cells in Ph-MPN (24). The gene discussed is SOAT1; the disease is myeloproliferative neoplasm.