Crispld1, also known as cysteine-rich secretory protein LCCL domain containing 1, belongs to the CAP superfamily. It may play roles in ion channel regulation, potentially in Ca2+ cycling based on its homology to ion channel regulatory toxins [2]. It is involved in multiple biological processes and is associated with various diseases, highlighting its biological importance. Genetic models, such as gene knockout models, can be valuable for studying its functions.

In gastric cancer, knockdown of Crispld1 reduces cell proliferation, invasion, and migration. It decreases intracellular calcium levels and inhibits the PI3K-AKT signaling pathway, indicating that Crispld1 promotes gastric cancer progression by mediating intracellular calcium levels and activating this pathway [1].

In heart failure, CRISPR/Cas9-mediated loss-of-function of Crispld1 in human-induced pluripotent stem cell-derived cardiomyocytes leads to dysregulated Ca2+ handling. Its down-regulation affects prohypertrophic, proapoptotic and Ca2+-signaling pathways, suggesting its contribution to adverse remodeling during the transition to heart failure [2].

In conclusion, Crispld1 is significantly involved in regulating biological processes related to calcium ion channels and signaling pathways. Model-based research, especially gene knockout experiments, has revealed its role in diseases like gastric cancer and heart failure. Understanding Crispld1 functions can potentially provide new therapeutic targets for these diseases.