SLC26A3 and spermatocele: As even none of the p.Val318del heterozygotes had spermatoceles reported in CLD8, heterozygous mutations of SLC26A3 along the male reproductive tract epithelia are likely to be tolerated, or compensated by other SLC26 transporters, as shown for SLC26A6 upregulation in the SLC26A3-defective intestine9.