Background: Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disorder characterized by persistent synovial inflammation, progressive joint damage, and debilitating functional impairment. The pathophysiology of RA is driven by complex interactions between genetic, immunological, and environmental factors, leading to dysregulated immune responses and aberrant cellular signaling pathways. Among these, the mammalian target of rapamycin (mTOR) pathway has garnered significant attention due to its central role in cellular growth, metabolism, and immune regulation. mTOR signaling influences key processes such as T-cell activation, macrophage polarization, synovial fibroblast proliferation, and the production of pro-inflammatory cytokines, all of which contribute to RA disease progression. Dysregulation of mTOR gene expression has been implicated in promoting synovial hyperplasia, angiogenesis, and the perpetuation of chronic inflammation in RA. This review comprehensively evaluates the current evidence on mTOR gene expression in RA, exploring its molecular mechanisms, functional consequences, and therapeutic implications. We analyze findings from preclinical studies, in vitro experiments, and emerging clinical trials investigating the use of mTOR inhibitors, such as rapamycin and its analogs, as potential disease-modifying agents. A deeper understanding of mTOR signaling in RA pathogenesis may pave the way for novel targeted therapies, offering improved outcomes for patients with this debilitating condition.