In our study, we explored the mechanistic basis for DDIT4-mediated regulation of GC cells using phospho-antibody microarray-based proteomic analysis and found that the proliferation-suppressive and chemosensitive effect of DDIT4 downregulation might be associated with activation of the MAPK signaling pathway, resulting in subsequent phosphorylation of BCL-2 (p-Ser70), which inhibits cell proliferation and induces apoptosis. The gene discussed is BCL2; the disease is gastric cancer.