Sickle cell disease (SCD) is a severe inherited blood disorder affecting about 100K US individuals, and blood transfusion is a key component in the clinical management of SCD patients. However, 8-76% SCD patients unfortunately become alloimmunized, many of which cause accelerated donor red blood cell destruction. Patients show substantial variability in their predisposition to alloimmunization, where genetic variability is one proposed component. Although several genetic association studies have been conducted for alloimmunization, the results have been inconsistent, and the genetic determinants of alloimmunization remain largely unknown. In an effort to advance genetic studies of alloimmunization, we performed a genome-wide association study (GWAS) in 236 African American (AA) SCD patients from the Duke OMG-SCD cohort, which is part of TOPMed, with whole genome sequencing data available. We applied logistic mixed models adjusting for sample relationship matrix and covariates, including presence of autoantibodies, hemoglobin genotype categories and sex. Despite the small sample size, we identified one genome-wide significant locus on chr12 (p = 3.1e-9) with no evidence of genomic inflation (lambda = 1.003). We also performed sensitivity analyses adjusting for additional covariates (Fyb antigen and the amount of blood transfusion) and applying different sample grouping strategies based on the number of alloantibodies patients developed (>=2 v.s. 0 and >=2 v.s. <=1). These analyses consistently revealed several additional suggestive loci. Furthermore, these suggestive loci are supported by both eQTL evidence from GTEx whole blood and/or Jackson Heart Study PBMC RNA-seq data, and 3D chromatin conformation information derived from HiC data in spleen and/or K562 cells. In conclusion, we identified several novel genetic variants that are significantly associated with alloimmunization among SCD patients and linked those variants to genes leveraging functional annotation information. We call for the community to collect additional alloantibody information within SCD cohorts to further the understanding of the genetic basis of alloimmunization in order to improve transfusion outcomes.