In OVCAR-3 human ovarian carcinoma cells, this compound inhibited cell growth, acting on parallel mechanisms: (1) at 20–30 μM concentrations, it enhanced the phosphorylation of the checkpoint kinase 2 (Chk2), which, in turn, activated intrinsic apoptosis independently of p53, increasing the Bax/Bcl-2 ratio; (2) theaflavin-3,3′-digallate (20 μM) caused G0/G1 arrest with an expected increase in p27 levels and a dramatic downregulation of CDK4, Cyclin D1, p-Rb, and Rb [173]. Here, RB1 is linked to ovarian carcinoma.