PEAK1, short for Pseudopodium-enriched atypical kinase 1, is a non-receptor tyrosine kinase that is involved in multiple cellular functions. It plays a role in signal transduction, connecting integrin and growth factor receptor signaling pathways. It has been implicated in processes like cell migration, proliferation, and apoptosis, and is thus of great biological importance in normal and disease-related contexts [2,3,5].

In breast cancer, high PEAK1 expression is associated with tumor size, grade, stage, lymph node metastasis, recurrence, and chemotherapy resistance. Inhibiting PEAK1 in breast cancer cells decreased growth, invasion, metastasis, and reversed chemoresistance [1].

In anaplastic thyroid carcinoma cells, targeting PEAK1 sensitized cells harboring BRAFV600E to vemurafenib by upregulating Bim and inducing apoptosis [4].

In colorectal cancer, some studies suggest that PEAK1-PPP1R12B axis inhibits tumor growth and metastasis through deactivation of the Grb2/PI3K/Akt pathway [5], while another study indicates its limited impact on colon carcinogenesis, potentially in the initial adenoma-to-carcinoma progression stage [7].

In pancreatic cancer, eIF5A-PEAK1 signaling regulates YAP1/TAZ protein expression, affecting 3D tumor sphere growth [6].

In neuronal cells after intracerebral hemorrhage, lncRNA-PEAK1 promotes apoptosis via the miR-466i-5p/caspase 8 axis [3].

In conclusion, PEAK1 is a crucial regulator in various biological processes, especially in cancer-related events such as tumor growth, metastasis, and chemoresistance. The functional studies using in vivo models, although limited in some cases, have provided insights into how PEAK1 contributes to these disease conditions, suggesting that targeting PEAK1 could be a potential therapeutic strategy in certain cancers and for intracerebral hemorrhage-induced neuronal apoptosis.