Hemophilia A and B are X-linked bleeding disorders commonly resulting from genetic alterations of the genes, F8 and F9. These genes encode Factor VIII and Factor IX of the coagulation cascade; deficiencies in one of these two factors define hemophilia A and hemophilia B, respectively. Numerous genetic variants in F8 and F9 have been identified.  The majority include single nucleotide variants (SNVs), copy number variants (CNVs), and in the case of F8, large intra-chromosomal inversions. Most CNVs have been found through analyses of targeted regions or techniques that detect differences in gene dosage. However, these methods cannot fully characterize the extent of each CNV as they are unable to detect breakpoints precisely. In this study, our goal was to characterize F8 and F9 CNVs in the My Life, Our Future hemophilia cohort that was recently whole genome sequenced (WGS) by the NHLBI TOPMed program. This cohort was mainly comprised samples from males diagnosed with hemophilia A (N=1,959) or hemophilia B (N=227). Comprehensive analysis of WGS data, revealed 64 CNVs in hemophilia A (57 deletions and 7 duplications) and 24 deletions in hemophilia B subjects. In hemophilia A, CNV size ranged from <100bp to > 100Kb and comprised single exon F8 deletions to multi-genic CNVs. Several F8 CNVs (N=14) included the first or last exon and exhibited heterogeneous breakpoints that differentially affected neighboring genes. In hemophilia B, CNV size ranged from approximately 1Kb to 6.5Mb and most included deletions of multiple exons or multi-genic deletions with substantial breakpoint heterogeneity. Most CNVs detected are causal for severe hemophilia (Factor VIII and Factor IX levels < 1%) and a subset of CNVs (N=16) are likely novel causal variants as they have not been previously reported. CNVs in two samples co-occurred with likely deleterious variants and a subset of CNVs co-occurred with likely benign missense variants. Together, these analyses demonstrate substantial heterogeneity in CNV size and breakpoint location. The identification of CNVs which impact a hemophilia gene and neighboring gene(s) may have clinical implications and raises the possibility of previously undetected hemophilia-associated syndromes. Moreover, combined analysis of SNVs and fully characterized CNVs will enable increased understanding of hemophilia presentation and complications.