However, researchers have now constructed and optimized the structure of a small ubiquitin-like modifier (SUMO)1 variant to obtain SUMO1, the segment including the hydrophobic binding pocket residues 15–55 [183], to interact multivalently with two SUMO-interacting motifs (SIM) located in the control of αSyn to exert stronger phase separation, inhibit αSyn aggregation, and improve the pathological manifestation of PD (Fig. 4). The gene discussed is SUMO1; the disease is Parkinson disease.