EGLN3 and neoplasm: Furthermore, the hydroxylase activity of PHD3 was also not required for the control of tumour growth, as expression of both wild-type PHD3 and PHD3 mutants with substitutions of critical residues in the catalytic hydroxylase domain, H196A and H135A/D137A3, 9, 20 similarly suppressed the growth of PHD3-deficient and control tumour cells (Fig. 5e, Supplementary Fig. 8c,d).