Our published work showed that Atmin modulates non-canonical Wnt/PCP signalling [27] and since Atmin affected Pkhd1 mRNA levels, the expression patterns of core and effector PCP proteins were examined in our previously characterised [18] normal (strong Fibrocystin expression) and ARPKD (no Fibrocystin expression, very large cysts) kidney tissues (Supplementary Fig. S5). Here, ATMIN is linked to autosomal recessive polycystic kidney disease.