A chip-based leukemia model revealed potential mechanisms of chemoresistance in the bone marrow microenvironment of B-cell acute lymphoblastic leukemia (B-ALL), where B-ALL cells utilize factors from the surrounding vasculature, endosteal, and hematopoietic microenvironment (e.g., CXCL12 cytokine signaling, VCAM-1/OPN adhesion signaling, and leukemia-specific NF-κB pathways) to maintain survival and quiescence [5]. This evidence concerns the gene NFKB1 and precursor B-cell acute lymphoblastic leukemia.