For PANS/ CANS/ PANDAS, autoantibodies are believed to target dopamine receptors in susceptible hosts (D1-, D2-dopamine receptors) through the process of molecular mimicry causing anti-D2R/ D1R imbalance and greater sensitivity to central dopamine signaling leading to subsequent activation of calcium calmodulin-dependent kinase (CAMK2) which is manifested clinically by the abrupt onset of movement (e.g., tics) or neuropsychiatric symptoms (e.g., OCD with rituals or tics) [2, 11]. This evidence concerns the gene DRD1 and Tics.