EVA1C, also known as eva-1 homolog C, is a protein-coding gene. It has been associated with axon guidance as it may account for some Robo-independent functions in the Slit/Robo axon guidance system, playing a role in the formation of neural circuitry in the developing mouse nervous system [3]. It also seems to be involved in Wnt signaling, with canonical Wnt signaling directly activating EVA1C as part of the mechanism that stops neuroblast migration [4].

In glioma, high EVA1C expression is linked to malignant clinicopathological features and poor overall survival, and is positively associated with immune infiltration levels of multiple immune cells, suggesting it could be a potential biomarker for predicting high immune infiltration in WHO grade II/III gliomas [1]. In neonatal hypoxic-ischemic encephalopathy (NHIE), EVA1C expression is upregulated in vitro after oxygen-glucose deprivation, and silencing EVA1C promotes neuron survival and growth, potentially associated with alternative splicing [2].

In summary, EVA1C plays important roles in neural-related processes such as axon guidance and neuron growth after injury. Its overexpression in glioma is related to poor prognosis and high immune infiltration, highlighting its significance in understanding and potentially treating these disease conditions. Research on EVA1C contributes to a better understanding of the underlying mechanisms of neural development-related diseases and glioma.