BCL2 and Sepsis: This SNHG1-DNMT1 binding mechanism with inactivation of p53, as depicted in Figure 5, has also been shown to promote sepsis-induced myocardial injury by inhibiting Bcl-2 expression, through recruitment of DNMT1 to the Bcl-2 promoter region, contributing to methylation of this gene, to promote the invasion of acute myeloid leukemia cells through recruitment of DNMT1 to the ZCCHC10 promoter region with subsequent inhibitory hypermethylation, and to promote the proliferation of gastric cancer cells [15,16,17].