fig1

Figure 1. Binding of BH3 mimetic, Venetoclax to BCL-2 anti-apoptotic protein releases bound BH3-only protein, subsequently allowing interaction between BH3-only protein and BAK/BAX. Upregulation of MCL-1, BCL-xL, and BCL2-A1 confers Venetoclax resistance by sequestration of BH3 only proteins, preventing them from interacting with BAK/BAX and avoidance of apoptosis^[35-40].