The basic deficiency of antenatal BS is the malfunction of mTAL chloride transport, which involves an interaction among the apical Na-K-2Cl cotransporter (NKCC2), the luminal ATP-sensitive potassium channel ROMK, the basolateral chloride channel (ClC), a basolateral K-CL cotransporter and the Na-K-ATPase. This evidence concerns the gene CLC and Bloom syndrome.