Thalassemia is a hematological disease caused by imbalanced globin production. The degree of diseases severity depends on several factors including the expression of fetal globin which can compensate for loss in adult globin. Genome wide association studies were performed to identify loci that are linked to reduction in disease severity. The majority of polymorphic sites are clustered within the globin genes. A subset of key loci is located at or near the genes encoding transcription factors functionally associated with globin gene expression. The polymorphism at the intergenic region between HBS1L and MYB was shown to one of the top severity modifying factors. A set of short transcripts corresponding to the intergenic HBS1L-MYB region was found in RNA-seq analyses of erythroid cell lines and hematologic stem cells, indicating that this intergenic region is actively transcribed. Recently, the enhancer RNA was shown to play roles in transcription control. These small non-coding RNAs might be responsible for change in disease severity. Quantitative RT-PCR was carried out to determine and quantify the non-coding HBS1L-MYB transcripts in primary human erythroblasts from normal individuals and Thalassemia patients. Three clusters of transcripts were identified. Interestingly, erythroblasts from beta-thalassemia/HbE patients have significantly lower levels of the non-coding transcripts than those from individuals with normal globin genes, warranting further studies to determine the function of these non-coding HBS1L-MYB transcripts.