Fuster et al. developed a TET2-deficient mouse model with increased progression of interleukin-1 beta-mediated atherosclerosis, while Sano et al. found that interleukin-1 beta expression was not increased in monocyte-lineage cells in which DNMT3a was knocked out by CRISPR, although the expression of interleukin-6 mRNA was increased [29,30]. The gene discussed is DNMT3A; the disease is atherosclerosis.