We have demonstrated that ASO-ANO1 could be used to inhibit the fixation of miR-9 on ANO1 mRNA by a target site blocker, and consequently to activate the alternative chloride channel to compensate CFTR Cl- deficiency regardless of the mutation (Sonneville et al., 2017). Here, ANO1 is linked to hyperinsulinemic hypoglycemia, familial, 4.