NFKB1 and acute promyelocytic leukemia: This was explained by EGCG ability to modulate oxidative stress activity inducing ROS production and bind to molecules leading to inhibition of enzymes activities (PIN1), modulation of signalling molecules (BCL-2, BAX, BAD, Cyclin D1, c-Myc, NF-κB p65, AKT) and modulation of receptors function (67LR), converging to the induction of apoptosis and differentiation in APL cells (Supplementary Fig. S6), thus providing new insights to the mechanisms of EGCG in leukaemia.