Cfl1, also known as cofilin, is a critical member of the actin depolymerizing factor (ADF) family. It plays a significant role in regulating actin cytoskeleton dynamics by cutting and depolymerizing actin filaments, which is essential for various biological processes such as cell migration, proliferation, and immune responses [2].

In chronic myeloid leukemia, the expression of Cfl1 was lower in patients compared to healthy controls and was upregulated after imatinib therapy. Lower Cfl1 expression before treatment was associated with a better response to imatinib, suggesting its potential as a predictor [1]. In hepatocellular carcinoma, Cfl1 is highly expressed in sorafenib-insensitive patients, and its knockdown can enhance the sensitivity of the cancer cells to sorafenib by remodeling serine synthesis and metabolism [3]. In gastric cancer, Cfl1 expression is increased, and its silencing by siRNA can inhibit cell migration and increase apoptosis, indicating it may function as an oncogenic gene [4].

In conclusion, Cfl1 is crucial for regulating actin cytoskeleton-related biological processes. Its study in disease models, such as in leukemia, liver cancer, and gastric cancer, has revealed its potential as a biomarker and therapeutic target, providing valuable insights into disease mechanisms and treatment strategies.