In vitro effects of C3G are well studied and it is known that C3G can suppress tumor cell proliferation by various mechanisms such as apoptosis induction [17], cell cycle inhibition [18], peroxidation inhibition [33] and migration inhibition [5,19], etc. Several signaling pathways have been implicated, such as inhibiting Ras signaling [16], down-regulating the expressions of CDKs [34], abolishing ethanol-mediated p130Cas/JNK interaction [19], elevating the Bax/Bcl-2 ratio [17], and inducing signaling by p38/p53 and c-jun [35]. Here, BCL2 is linked to neoplasm.