Although the probable involvement of other inflammatory pathways in diabetogenesis [e.g., the c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB), tumor necrosis factor (TNF) pathways] and the highly selective study participants as well as potential lifestyle changes in the specific population were supposed to account for the overall inefficiency of canakinumab [6, 36] for diabetes prevention, our findings provided another explanation for the discouraging result. The gene discussed is TNF; the disease is diabetes mellitus.