In Longmin's work, they found that loss of Kdm2a promotes Pparg transcription by inhibiting its H3K36me2 demethylation, thereby protecting against from high fat diet-induced obesity.18 In addition, KDM2A can promote the de-clustering of alternative telomere elongation to sustain the replicative immortality of tumor cells 23. The gene discussed is KDM2A; the disease is obesity disorder.