As an atypical member of the Rho family small GTPases, RhoH shares less than 50% sequence similarity with other members, and its expression is commonly observed in the haematopoietic lineage. To date, RhoH function was observed in regulating T cell receptor signalling, and less is known in other haematopoietic cells. Its activation may not rely on the standard GDP/GTP cycling of small G proteins and is thought to be constitutively active because critical amino acids involved in GTP hydrolysis are absent. Alternatively, its activation can be regulated by other types of regulation, including lysosomal degradation, somatic mutation and transcriptional repressor, which also results in an altered protein expression. Aberrant protein expression of RhoH has been implicated not only in B cell malignancies but also in immune-related diseases, such as primary immunodeficiencies, systemic lupus erythematosus and psoriasis, wherein its involvement may provide the link between immune-related diseases and cancer. RhoH association with these diseases involves several other players, including its interacting partner, ZAP−70; activation regulators, Vav1 and RhoGDI and other small GTPases, such as RhoA, Rac1 and Cdc42. As such, RhoH and its associated proteins are potential attack points, especially in the treatment of cancer and immune-related diseases.

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The role of RhoG in T cell development is redundant with other Racs subfamily members, and this redundancy may be attributed to redundant signal transduction pathways. However, the absence of RhoG increases TCR signalling and proliferation, implying that RhoG activity is critical during late T cell activation following antigen–receptor interaction. Moreover, RhoG is required to halt signal transduction and prevent hyper-activated T cells. Despite increase in TCR signalling, cell proliferation is inhibited, implying that RhoG induces T cell anergy by promoting the activities of transcription factors, including nuclear factor of activated T cell (NFAT)/AP-1. The role of NFAT plays in T cell anergy is inducing the transcription of anergy-associated genes, such as IL-2, IL-5, and IFN-γ. Although information about RhoG in T cell-related diseases is limited, mutant forms of RhoG, Ala151Ser and Glu171Lys have been observed in thymoma and hemophagocytic lymphohistiocytosis (HLH), respectively. Current information only focuses on these two diseases, and thus the role of RhoG in normal and pathological circumstances should be further investigated. This approach is necessary because RhoG and its associated proteins represent prospective targets for attack particularly in the therapy of cancer and immune-mediated illnesses.

The emergence of antibiotic resistance among pathogenic microorganisms is a major issue for global public health, as it results in acute or chronic infections, debilitating diseases, and mortality. Of particular concern is the rapid and common spread of carbapenem resistance in healthcare settings. Carbapenems are a class of critical antibiotics reserved for treatment against multidrug-resistant microorganisms, and resistance to this antibiotic may result in limited treatment against infections. In addition to in clinical facilities, carbapenem resistance has also been identified in aquatic niches, including marine environments. Various carbapenem-resistant genes (CRGs) have been detected in different marine settings, with the majority of the genes incorporated in mobile genetic elements, i.e., transposons or plasmids, which may contribute to efficient genetic transfer. This review highlights the potential of the marine environment as a reservoir for carbapenem resistance and provides a general overview of CRG transmission among marine microbes.

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