Previously, our group showed that expression of CYP enzymes appears to be at least partly responsible for the well‐recognized ability of BMSCs to protect AML cells from chemotherapy.8, 10 The BM during leukaemia therapy is a dynamic environment with changes related to treatment and tumour burden; we suggested that these changes likely can modulate drug metabolizing enzymes in the BM microenvironment, and as a consequence, drug resistance. The gene discussed is PPIG; the disease is neoplasm.