TIM3 also showed high expression levels in other hematological malignancies, and our team found that high expression of TIM-3 was present on myeloma cells of multiple myeloma (MM) patients and correlated with disease progression, and was also found to be closely related to the activation of the NF-κB signaling pathway; knockdown of TIM-3 significantly inhibited cell proliferation and induced apoptosis, and bortezomib had a synergistic NF-κB pathway inhibition, suggesting that TIM-3 could be a potential future therapeutic target for MM (34). The gene discussed is NFKB1; the disease is AL amyloidosis.