However, the most compelling reason to target the Id1/Kif11 pathway came from work [23] that identified the drug BRD9876 as a kinesin-5 inhibitor in multiple myeloma, which led to significant downregulation of ID1. On the basis of our work, we used Id as a marker for the chemoresistant CSC population in TNBC. Here, ID1 is linked to AL amyloidosis.