Rab27b, a member of the Rab family of small GTPases, plays crucial roles in endocytosis, exocytosis, and vesicle trafficking [5]. It is involved in multiple cellular processes such as exosome secretion, which is essential for intercellular communication and is associated with various physiological and pathological conditions [2].

In myeloid leukemia, Rab27b deficiency in mice abrogated mutant NRAS-mediated progenitor cell growth, ERK signaling, and NRAS palmitoylation, and significantly reduced myelomonocytic leukemia development in vivo. It controls NRAS palmitoylation and trafficking to the plasma membrane for activation, and its upregulation in CBL-or JAK2-mutated myeloid malignancies correlates with poor prognosis in acute myeloid leukemias (AMLs) [1].

In endometriosis, silencing Rab27b in ESCs can inhibit cell proliferation, migration, invasion, and angiogenesis-related functions [3].

In pancreatic cancer, ZIP4 promotes muscle wasting and cachexia by activating CREB-regulated expression of Rab27B, which is required for the release of extracellular vesicles from pancreatic cancer cells [4].

In NSCLC, knockdown of RAB27B in NSCLC CSCs leads to a loss of stem-cell-like phenotypes [6].

In gastric cancer, knockdown of Rab27b in 58As9 cells decreased peritoneal metastases in vivo [7].

In conclusion, Rab27b is a key regulator in multiple biological processes. Gene-knockout studies in mice have significantly contributed to understanding its role in diseases like myeloid leukemia, endometriosis, pancreatic cancer-associated cachexia, NSCLC, and gastric cancer peritoneal metastases, providing potential therapeutic targets for these diseases.