We used sufficient experimental evidence to demonstrate that the advanced glycation end-product Nε-carboxymethyl-lysine (CML) promotes foam cell apoptosis (Figure 2) in diabetic atherosclerotic plaques through classic apoptosis pathways (Bcl-2/Bax, caspase-3 and caspase-9) in a concentration-dependent manner, and we suggested that the underlying mechanism involved inhibition of the PI3K/Akt signaling pathways (Wang et al., 2019). Here, PIK3CA is linked to diabetes mellitus.