Here, we present a neonate with classical salt-wasting 21-OHD due to a point mutation I2A/C656G of [i]CYP21A2[/i], which is one of the most frequent mutations in the classic 21-OHD and causes premature splicing of the intron and a shift in the translational reading frame (5). Here, CYP21A2 is linked to classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency.