The study revealed that the mechanism involves in the GM–CSF-mediated generation of the IL-23, where adds apoptosis sensitivity to macrophages through increasing the proteasomal degradation of the cell-survival protein B-cell lymphoma-2 (Bcl-2) along with oxidative stress in the LDL-driven atherosclerosis (Tausend et al., 2014). The gene discussed is BCL2; the disease is atherosclerosis.