These discrepancies could be explained by at least three reasons: our cohort was larger than the one used in the previous study (214 vs 23) as well as the control group of PBHV (20 vs 5); the qPCR control in the previous study was GAPDH, while we used PPIA, which is more stable in CLL; and finally, based on the reverse TET2 primer (the forward has been mistaken for the GAPDH reverse primer), their amplicon was in the 3' region (nucleotide 8941 to 8960), while ours was further upstream (nucleotide 4367 to 4389) which is a region less sensible to RNA degradation. The gene discussed is TET2; the disease is B-cell chronic lymphocytic leukemia.