In line with this observation, Kuepper et al. reported that IL6 could be a trigger of a JAK1-STA3 signaling pathway activation leading to the persistence of CML-LSCs; in this context, the use of JAK1 specific inhibitors (Filgotinib and Itacitinib) in combination with BCR-ABL inhibition induced apoptosis in quiescent CML-LSCs [41]. The gene discussed is JAK1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.