SRP354598 PRJNA756128 Pfkm knockout mice Genome sequencing Celastrol were one of the most powerful leptin sensitizer. We discovered that celastrol directly bound and inhibited PFKM. To verify if PFKM is responsible for leptin sensitization, we generated this mice using Crispr-cas9 mediated homologous recombination. Considering that Pfkm deficiency might cause embryonic lethality, we attempt to introduced the Cre-loxP system to achieve Pfkm conditional knockout. Two loxp sites were successfully inserted at upstream of exon 5 and downstream of exon 6, to our surprise is that the homozygous Pfkm KO mice totally lacked PFKM expression in skeletal muscle, liver, and hypothalamus. This is the whole genome sequencing data of Pfkm knockout mice and their wild-type littermate. The results indicated that loss of PFKM in Pfkm knockout animals is caused by loxP insertion rather than the off-target of Crispr-cas9 editing. Mus musculus strain:C57BL/6J-Pfkm^em1TC