Syngr4, also known as synaptogyrin-4, is a gene whose role has been implicated in multiple biological contexts. While its exact core function and associated pathways are still being elucidated, studies suggest it may be involved in processes related to motor neuron function, cancer development, and potentially coronary artery disease [1-4].

In amyotrophic lateral sclerosis (ALS) models, the deregulation of Syngr4 at both the mRNA and protein levels has been observed in motor neurons of TDP-43-driven ALS mouse models. This spatial and temporal pattern of deregulation implies that Syngr4 could be functionally important in driving the transition to the symptomatic phase of the disease [1,2].

In breast cancer, Syngr4 is highly expressed, affecting breast cancer prognosis, proliferation, migration, and tumor-associated macrophage polarization towards M2, suggesting it could be a novel target for immunotherapy [3].

In coronary artery disease, Syngr4 was identified as a differentially expressed gene in one of the subtypes, with functional analyses indicating its involvement in cellular functions related to responses to metal ions and inorganic substances, and enriched in inflammation and hormone-related pathways [4].

In conclusion, Syngr4 appears to play diverse roles in different biological processes and disease conditions. The findings from ALS mouse models, breast cancer studies, and coronary artery disease research suggest its importance in motor neuron function, cancer development, and potentially in the pathophysiology of coronary artery disease. These studies using various research models, such as mouse models in ALS, provide valuable insights into the functions of Syngr4, helping to understand the underlying mechanisms of these diseases and potentially leading to new therapeutic strategies.