Rras, also known as R-Ras, is a small monomeric GTPase that plays a crucial role in regulating cell adhesion, spreading, and migration [5]. It is involved in the RAS/mitogen-activated protein kinase (MAPK) pathway, which is significant in cell cycle regulation [3,5].

In the context of lung fibrosis, endothelial-specific Foxf1 inhibition in mice led to impaired R-Ras signaling, increased collagen depositions, and promoted lung inflammation. FOXF1 was found to inhibit TNFα and CCL2 through direct transcriptional activation of the Rras gene promoter [1].

In bladder cancer, the METTL3/YTHDF2 m6A axis epigenetically suppresses RRAS, promoting the malignant progression of the cancer. METTL3 binds to the m6A sites of RRAS mRNA, suppressing its transcriptional activity, and YTHDF2 mediates RRAS degradation [2].

In nasopharyngeal carcinoma, the expression of RRAS was down-regulated and was associated with poor prognosis. RRAS suppressed the proliferation, invasion, and epithelial-mesenchymal transformation of NPC cell lines, suggesting it may act as a tumor suppressor gene [4].

In conclusion, Rras is a key regulator in multiple biological processes and disease conditions. Mouse models and in vitro cellular experiments have revealed its significance in lung fibrosis, bladder cancer, and nasopharyngeal carcinoma, among others. These findings enhance our understanding of the role of Rras in disease pathogenesis and may provide potential therapeutic targets for these diseases.