Fkbp1a, also known as FKBP12, is a ubiquitously expressed cis-trans peptidyl-prolyl isomerase. It is involved in multiple biological processes. It has been linked to pathways such as the apoptosis pathway and mTOR signaling pathway, and is critical for various tumors and cancers [1,2,3]. Genetic models, especially gene knockout (KO) models, are valuable for studying its functions.

In a KO mouse model, Fkbp1a-deficient mice develop ventricular hypertrabeculation and non-compaction. Endothelial cell-restricted ablation of Fkbp1a recapitulated this defect, suggesting Fkbp1a within the developing endocardia is important in regulating ventricular trabeculation and compaction. Fkbp1a was found to be a negative modulator of activated Notch1, with its ablation leading to upregulation of activated Notch1 (N1ICD) [4]. In glioblastoma cell lines, upregulated Fkbp1a promoted cell death, inhibiting glioblastoma growth via the apoptosis pathway [1].

In conclusion, Fkbp1a plays essential roles in processes like ventricular wall formation and tumor-related cell growth regulation. Gene knockout mouse models have revealed its functions in these specific biological and disease-related areas, contributing to a better understanding of related physiological and pathological mechanisms.