Zfpm1, also known as Friend of GATA1 (FOG-1), is an essential transcriptional co-factor. It is involved in multiple biological processes, playing a crucial role in cell differentiation, development, and in maintaining cellular homeostasis. It associates with GATA transcription factors and is part of the regulatory machinery for gene expression in various cell lineages [4,5].

In zebrafish, zfpm1 knockout leads to compromised cardiac function with deformed trabecular meshwork. The loss of Zfpm1 activity results in over-activation of Neuregulin-ErbB signalling and abnormally elevated cardiomyocyte proliferation during cardiac trabeculae growth and modelling stages, indicating its role in coordinating trabeculae patterning and growth [1].

In mice, conditional knockout of Zfpm1 affects the development of dorsal raphe serotonergic neuron subtypes. In perinatal and adult mutants, there are changes in the number of serotonergic neurons in different subpopulations of the dorsal raphe nucleus, reduced serotonin concentration in rostral brain areas, increased anxiety-like behavior, and in female mutants, elevated contextual fear memory [3].

In breast cancer research, next-generation sequencing of encapsulated papillary carcinoma (EPC) reveals that 21.9% of EPCs have somatic ZFPM1 mutations, often concurrent with PI3K-AKT-mTOR pathway mutations, suggesting a role in this specific cancer type [2].

In conclusion, Zfpm1 is vital for normal development, especially in cardiac trabeculation and the development of serotonergic neuron subtypes. The study of Zfpm1 knockout and conditional knockout models in zebrafish and mice has provided insights into its role in cardiac function and mood-related behaviors. In addition, the discovery of ZFPM1 mutations in EPC indicates its potential significance in breast cancer. These model-based studies contribute to understanding the biological functions of Zfpm1 and its implications in disease.