Furthermore, in CML, stromal cells appear to play a critical role in maintaining LSC dormancy partly through the bone morphogenetic protein 4 (BMP4)-BMP receptor 1B (BMPR1B) pathway, cooperating with JAK2/STAT3 signaling to induce quiescent gene expression and lead to residual LSC persistence [95]. The gene discussed is JAK2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.