Mice are skttish creatures that innately hide from perceived threats by staying out of open areas, freezing to avoid predators, or hiding in dark spaces when an adverse stimulus is sensed. However, after inducing a global TPPP (tubulin polymerization promoting protein) gene knock-out (KO), which results in reduced myelin length and thickness (Fu et al., 2019), Nguyen et al. (2020) found that these natural behaviors become less pronounced (Fig. 1). They also report that fear conditioning is less effective in the Tppp KO mice, indicating that their ability to learn to fear a specific event is impaired. Fear impacts many brain circuits and is critical for survival, but the contribution of non-neuronal cells in fear circuits is not well understood. This work identifies a protein that influences both innate and learned fear via its role in microtubule nucleation in oligodendrocytes. Figure 1. A ) Normal branching and myelin sheath length in oligodendrocytes in WT mice is coupled with normal fear conditioning and innate fear responses. B ) Tppp KO results in highly branched oligodendrocytes with shorter, thinner myelin sheaths. These mice have dramatically reduced fear conditioning and innate fear responses. In the cell body of most cells, microtubules are nucleated from perinuclear centrosomes. These microtubule organizing centers (MTOCs) contain centrioles and a pericentriolar matrix containing g-tubulin ring complexes (γTURCs). γTURCs are the starting point for the initiation and subsequent polymerization of α/βtubulin dimers into cytoplasmic microtubules. Golgi outposts are a different type of MTOC that nucleate microtubules outside of the cell body in …