Our work also identified biologically relevant genes for hematological traits at loci not containing previous GWAS signals, as well as genes which may explain known GWAS signals in gene-dense regions or highlight additional sub-genome-wide significant conditionally distinct signals at known loci, such as TNFAIP2. Previous studies reported that TNFAIP2, identified by TWAS with the MESA HL reference panel for platelet count, is related to acute promyelocytic leukemia [58,59] and may play a role as mediator of inflammation [60] and angiogenesis [61]. This evidence concerns the gene TNFAIP2 and acute promyelocytic leukemia.