We think that the reason why knocking down KDM6A in the lowly expressing PLC/PRF/5 cells still showed the tumour growth‐inhibiting effects was presumably due to the residual expression of KDM6A in PLC/PRF/5, which remains to function to a large extent to promote PLC/PRF/5 cells proliferation ability. This evidence concerns the gene HSPG2 and neoplasm.