Acetylated microtubules are far more stable and resistant to drug-induced depolymerization than non-acetylated microtubules.4 Furthermore, one of the mechanisms of acquired resistance to microtubule inhibitors involves the expression-mediated upregulation of TUB isotypes, which inhibit the actions of these agents.3 For this reason, microtubule inhibitors fail to affect microtubule dynamics effectively when microtubule destabilizing agents are employed in an anti-cancer strategy. Here, TUB is linked to cancer.