Dock6, a guanine nucleotide exchange factor (GEF) for Rac1 and CDC42, plays significant roles in multiple biological processes. It is involved in pathways such as the WNT/β -catenin signaling pathway, which is crucial for cell growth, differentiation, and development. Genetic models, like KO/CKO mouse models, are valuable for studying Dock6's functions and its implications in diseases [1].

In gastric cancer, Dock6 promotes chemo-and radioresistance by modulating WNT/β -catenin signaling and cancer stem cell traits. Its elevated expression is associated with poor prognosis [1]. In oral squamous cell cancer, Dock6 is upregulated, promoting cellular migration and invasion, also related to a poor prognosis [3]. In Adams-Oliver syndrome, autosomal recessive DOCK6-related forms often lead to severe phenotypes including central nervous system and ocular abnormalities, with intrafamilial phenotypic variability observed [2,4].

In conclusion, Dock6 is a key factor in cell-signaling pathways, influencing processes related to cancer progression and certain genetic syndromes. Studies using KO/CKO mouse models could potentially further clarify its functions and contribute to the understanding of related disease mechanisms, providing insights for possible therapeutic interventions in cancer and genetic disorder management.