The overexpression of TCP1/CCT2/CCT3/CCT4/CCT5/CCT6A is related to the abnormal regulation of the Myc target gene, hypoxia-inducible factor target gene, and cell cycle, especially the G1max S transition.[29] In blastoma, the expression mutation of CCT family genes, in which CCT6A has the most incredible expression mutation and amplification induction in blastoma, has a negative correlation with survival rate.[30]. This evidence concerns the gene CCT2 and blastoma.