Further, silencing of miRNA-485-5p resulted in a significant increase in the expression of the target gene, ATP6V1C2, levels of which were 4.121-fold higher in infants with SAE than that in preterm infants without encephalopathy after sepsis (p < 0.05) (Fig. 5A, B). Here, ATP6V1C2 is linked to Encephalopathy.