In May, Tiffany Terry successfully defended her thesis, “The role of IGF1 signaling in the development of cerebellar granule cells.” Her work in Hui Zong’s lab focused on determining whether IGF1 signaling was necessary for the development of normal granule cell progenitors (GCPs) since IGF1 was identified as a crucial niche factor that promoted the proliferation of medulloblastoma tumor cells, which are derived from GCPs. Using the mouse genetic system called Mosaic Analysis with Double Markers (MADM), she discovered that IGF1 signaling is critical for the development of normal GCPs since the loss of the IGF1 receptor led to a significant reduction in the number of granule cells produced in the cerebellum. Then, she determined that IGF1 signaling specifically regulates the cell cycle progression of normal GCPs. When IGF1 signaling is lost, GCPs prematurely exit the cell cycle contributing to the reduced number of granule cells produced. Lastly, she identified the cell type in the cerebellar environment that secreted IGF1 and the temporal pattern of IGF1 expression during cerebellar development. Based on these studies, it is conceivable that the IGF1 signaling pathway’s inhibition could enhance the suppression of medulloblastoma progression. However, the dual role of IGF1 signaling on GCP development and medulloblastoma progression warrants caution since the tumor arises during cerebellar development.