Laboratory and epidemiological studies have shown that short sleep time is associated with obesity. In this study, we conducted a post-GWAS analysis to test genetic correlation between children's sleep and obesity due to linkage disequilibrium (LD) SNPs, shared genes and pathways. Our analysis showed that genetic heritability was 0.14 (p-value = 0.0005) and 0.41 (p-value = 1.18E-24) for children's sleep and obesity, respectively, but genetic correlation due to LD SNPs was insignificant. Gene associations at children's GWAS were measured based on SNP associations and ranked by their uniform score (U-score). After adjusting for gene size, measured as the number of independent SNPs, children's sleep and obesity GWAS had significant gene correlation (r = 0.23). Pathway enrichment analysis showed that "Suz12 target genes" was the significant pathway for both children's sleep and obesity; pathways were significantly shared among top enriched pathways with an OR of 8.1-59.4; and significant correlation coefficient of pathway U-score was r = 0.36. Analysis of sleep time and obesity GWAS variants for all ages in the NHGRI-EBI GWAS Catalog also presented significant pathway correlation (r = 0.30). The "PAX3-FOXO1 target genes" was the significant pathway for all-age obesity phenotype and ranked as the second top associated pathway for all-age sleep time. Our study suggested that genetic correlation of children's sleep time and obesity is attributed to genes with pleiotropy effects and common pathway regulations that may contain only weak SNP associations.