Peled et al. demonstrated that disrupting the CXCL12/CXCR4 axis using motixafortide is an effective way to abrogate the BM-derived mesenchymal stem-cell-mediated resistance of nHL cells to rituximab and to target nHL in the BM microenvironment [139]. This evidence concerns the gene CXCL12 and non-Hodgkin lymphoma.