Overall, we deduced under the condition of coronary artery anoxia that miR-127 not only enhanced VEGFA secretion and SOCS3 promoter methylation but also inhibited the expression of SOCS3 through the JAK/STAT3/NF-κB pathway, leading to pathological angiogenesis, which was involved in left ventricular injury, coronary artery hyperplasia, and restenosis after MI, consistent with the research conclusion of Boosani et al. [48]. The gene discussed is NFKB1; the disease is myocardial infarction.