Muchowski et al. found the essential role of microtubule networks in inclusion body formation in a yeast model of HD, and demonstrated that treatment of yeast with chemicals that disrupt microtubule networks, however, facilitates the polyQ-induced toxicity: perturbation of microtubule-dependent intracellular trafficking results in suppression of inclusion body formation, leading to an increase in the levels of huntingtin protein in a soluble, non-aggregated form [46]. Here, HTT is linked to Huntington disease.