Our finding that EPO induction in the presence of an additional stimulus, such as anaemia, is restricted to the cortex, even in animals with PDGFR‐β‐specific PHD3 deletion, also argues against both compensatory PHD3 upregulation as the underlying mechanism for the lack of medullary EPO production and a role of PHD3 in general (Fig. 8). This evidence concerns the gene PDGFRB and anemia (phenotype).