SETD2 deficiency is associated with metabolism of three major substances, including carbohydrate, glycosaminoglycan and creatine 11, and SETD2-inactive cells are likely to enhance the PGC1α expression at the protein (PGC1α has been known as a stimulator in tumor of digestive system66) level and undergo a higher level of tricarboxylic acid cycle process with released energy. Here, PPARGC1A is linked to neoplasm.