Knockdown of CCN4 in the cell line with the highest expression inhibited proliferation and induced apoptosis by down-regulating expression of, amongst others, p-AKT, p-ERK and Bcl-2, and upregulation of Bax, suggesting a possible pro-leukemic effect of CCN4 in T-ALL (Fig. 4b) (Zhang et al. 2015). The gene discussed is BCL2; the disease is acute lymphoblastic leukemia.