However, it was demonstrated by [31] that no significant differences were found in transcript levels of c-Kit in a mouse model of Huntington disease, another polyglutamine disease, when compared with control mice, upon treatment with PLX3397, supporting the notion that the drug effects in this model were due specifically to the inhibition of microglial CSF1R and subsequent microglial depletion [31]. Here, CSF1R is linked to juvenile Huntington disease.