Using wild-type and periostin-deficient transgenic mice in a BALB/c background, the researchers revealed that BM-derived MSC expressed higher levels of periostin (via STAT3 activation) when co-cultured with B-ALL cells and that periostin deficiency in MSC decreases CCL2 expression in co-cultured B-ALL cells; CCL2 expression in these cells is regulated by the ILK/NF-kB pathway [166]. This evidence concerns the gene CCL2 and precursor B-cell acute lymphoblastic leukemia.