The crystal structures of PPT1 and PPT2 reveal that although both have similar architectural features, conformational differences near the active site partially explain substrate selectivity, as the entrance space of the lipid binding site consisting of β3-αA and β8-αF in PPT1 is larger than that in PPT2 and thus more inclusive of the substrates.71 Deficiency of PPT1 or PPT2 results in serious neurodegeneration, while overexpression of PPT1 or PPT2 may accelerate tumour growth.72–75. The gene discussed is PPT1; the disease is neoplasm.