In line with our study, Yoshikane Kikushige et al. in 2015 represented that expansion and transformation of malignant myeloid clones could happen through ligation of TIM-3/Gal-9 and induction of the NF-κB and β-catenin signaling pathway at the same time through its autocrine loop which caused in production of leukemia transformed models from MDS, Myeloproliferative neoplasms (MPN), and also in de novo AML [52]. The gene discussed is NFKB1; the disease is myelodysplastic syndrome.