We speculate that the riboflavin deficiency in ESCC cells increases TNFα and activates NF-κB, which increases the expression of SLC52A3, providing a mechanistic explanation for the negative feedback regulatory mechanisms maintaining riboflavin homeostasis inferred from the previous studies [9, 54]. Here, NFKB1 is linked to hyperinsulinemic hypoglycemia, familial, 4.