Numerous cancer types are affected by STIL overexpression which has been linked to chromosomal instability. It plays a part in neural development and function. STIL plays a crucial role in cell mitosis and centriole replication. The early stages of the cell cycle see a slow increase in STIL expression, a peak in the middle, and a sharp decline in the latter stages. When cellular proliferation is inhibited by serum deprivation, contact inhibition, or the promotion of terminal differentiation, STIL is expressed in the proliferating cells and is down-regulated. STIL has been interacted with CDK1, PLK4, and SAS-6. STIL has a role in the Sonic hedgehog (Shh) pathway. STIL regulates the transcription of Shh-target gene Gli1.The suppressor-of-fused homolog (SUFU) and GLI1 are examples of conserved Shh signaling elements with which the C terminus of STIL can engage. The activation of Shh-GLI1 cascades is caused by STIL's interaction with SUFU, which prevents SUFU from acting as a repressor of GLI1.