The possible mechanisms behind that were upregulation of Chemokine receptor type 4 (CXCR4), the direct target of miR-195-5p, enhancement of superoxide dysmutase SOD, inhibited in TAC group, and subsequent inhibition of Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway activation (Figure 2) [34]. The gene discussed is SOAT1; the disease is persistent truncus arteriosus.