Cytoskeleton proteins, such as actin and tubulin, are known substrates of CCTs.[39] According to one study, deletion of CCT8 suppressed the formation of nuclear actin filaments in T cells, affecting T cell maturation and function.[40] Furthermore, CCT8 influenced the migration and invasion of ESCC cells by regulating the expression of α-actin and β-tubulin in esophageal squamous cell carcinoma.[16] Additionally, interactions between CCTs and other functional proteins were reported. This evidence concerns the gene CCT8 and esophageal squamous cell carcinoma.