β-thalassemia is caused by β-globin gene mutations.However,heterogeneous phenotypes were found in individuals with same genotype,and still undescribed mechanism underlies such variation.We collected blood samples from 30 β-thalassemia major,30 β-thalassemia minor patients,and 30 matched normal controls.Human lncRNA Array v2.0 (8 × 60 K,Arraystar) was used to detect changes in long non-coding RNAs (lncRNAs) and mRNAs in three samples each from β-thalassemia major,β-thalassemia minor,and control groups.Compared with normal controls,1424 and 2045 lncRNAs were up-and downregulated,respectively,in β-thalassemia major patients,whereas 623 and 349 lncRNAs were up-and downregulated,respectively,in β-thalassemia minor patients.Compared with β-thalassemia minor group,1367 and 2356 lncRNAs were up-and downregulated,respectively,in β-thalassemia major group.We selected five lncRNAs that displayed altered expressions (DQ583499,X-inactive specific transcript (Xist),lincRNA-TPM1,MRFS16P,and lincRNA-RUNX2-2) and confirmed their expression levels in all samples using real-time polymerase chain reaction.Based on coding-non-coding gene co-expression network and gene ontology biological process analyses,several signaling pathways were associated with three common organ systems exhibiting β-thalassemia phenotypes:hematologic,skeletal,and hepatic systems.This study implicates that abnormal expression levels of lncRNAs and mRNA in β-thalassemia cases may be correlated with its various clinical phenotypes.