Interestingly, in a subsequent study the same authors showed that soluble galectin-9 is increased in the serum of AML patients and that it binds to TIM-3 expressed on LSCs, inducing an autocrine stimulatory loop that promotes LSC self-renewal via NF-κB and β-catenin signaling (210). The gene discussed is HAVCR2; the disease is acute myeloid leukemia.