SIX1 and cancer: For instance, α-synuclein (S129D/E) did not imitate the structure and aggregation characteristics of truly phosphorylated α-synuclein.62 Protein kinase B/AKT (T308D/E) did not activate its substrates like authentically phosphorylated AKT.63 In our study, SIX1 (S225D/E) also failed to mimic really phosphorylated SIX1 in terms of regulation of glycolytic gene expression, production of lactate and ATP, cancer cell proliferation and invasion, and tumor growth and metastasis.