YWHAQ, also known as 14-3-3 tau, is a member of the 14-3-3 family of proteins. These proteins play crucial roles in various cellular processes such as signal transduction, apoptosis, and cell cycle regulation by binding to phosphorylated proteins [1,3,4,5]. They are involved in multiple signaling pathways, influencing cell survival and function. Genetic models, like KO/CKO mouse models, can be valuable for further exploring its functions.

In breast cancer, miR-16-5p can target YWHAQ, regulating apoptosis and migration of paclitaxel-resistant breast cancer cells. By modulating YWHAQ, miR-16-5p affects the expression of Bcl-2 and Bax, thereby altering the biological behaviors of these cells [1].

In preeclampsia, the YWHAQ promoter shows hypermethylation in the placenta, and the expression of 14-3-3 tau (YWHAQ) is down-regulated, suggesting its involvement in the molecular mechanisms of this disorder [2].

In amyotrophic lateral sclerosis (ALS), the YWHAQ transcript is significantly up-regulated in the lumbar spinal cord of patients, indicating its potential role in a 14-3-3-mediated survival pathway in ALS pathogenesis [3].

In left ventricular non-compaction cardiomyopathy (LVNC), SORBS2 interacts with YWHAQ, having a negative effect on the cell cycle, potentially leading to LVNC [4].

In hepatocellular carcinoma (HCC), RFX5 transactivates YWHAQ, and the RFX5-YWHAQ pathway suppresses apoptosis, promoting HCC progression [5].

In conclusion, YWHAQ is involved in multiple biological processes and disease conditions. Studies on YWHAQ, especially through gene-knockout models, have provided insights into its roles in breast cancer, preeclampsia, ALS, LVNC, and HCC. Understanding YWHAQ's functions may offer new strategies for treating these diseases.