Having shown that the FEN1/POLβ molar ratio is 1.4+/−0.3 in the striatum and 6+/−1.2 in the cerebellum of R6/1 mice (Figure S3B), that FEN1-like nuclease activity is 5- to 10-fold more elevated in the cerebellum (Figure 4C), and that POLβ is specifically enriched at CAG expansions in the striatum of HD mice (Figure 5), we suspected that the FEN1/POLβ ratio might be critical in determining the propensity of a given tissue to experience somatic CAG instability. Here, POLB is linked to Huntington disease.