Nerve Growth Factor (NGF) plays a dual role in inflammation and cancer, acting as both a pro-inflammatory and oncogenic factor, and as an anti-inflammatory and pro-apoptotic mediator depending on the context. This review summarizes the literature on NGF's role in regulating the inflammatory microenvironment and tumor cell growth, survival, and death. NGF is a neurotrophic factor involved in the growth, survival, and maintenance of neuronal and non-neuronal cells. It belongs to the family of neurotrophins, including BDNF, NT-3, and NT-4/5. NGF is synthesized as pro-NGF, which can have pro-apoptotic effects. NGF acts through two main receptors: TrkA and p75NTR. TrkA is a high-affinity receptor that activates signaling pathways involved in cell growth and survival, while p75NTR modulates NGF signaling and can influence cell death and survival. NGF can also interact with other receptors like sortilin and neuropilin-1, which are involved in cancer growth. Inflammation is a complex biological response that can contribute to tumor development and progression. Chronic inflammation can promote tumor initiation, growth, and metastasis by fostering angiogenesis, ECM remodeling, and immune suppression. NGF can influence inflammation by modulating immune responses and interacting with immune cells. NGF has been shown to support the survival and functionality of various immune cells, including mast cells, lymphocytes, macrophages, and natural killer cells. NGF can also promote the expansion of regulatory T cells, which can suppress the anti-tumor immune response. NGF plays a significant role in various aspects of cancer, including tumor growth, survival, and metastasis. It can promote tumor progression by stimulating cancer cell proliferation and suppressing apoptosis. NGF can also induce epithelial-mesenchymal transition (EMT), increasing cell mobility and invasiveness. NGF can influence the tumor microenvironment (TME) by modulating immune responses, angiogenesis, and the survival of cancer cells. NGF can also modulate the expression of cytokines and chemokines in the TME, influencing the function of immune cells and creating an immunosuppressive environment that favors tumor growth. NGF receptor expression in cancer varies, with Trk and p75NTR receptors playing significant roles in different types of cancer. Aberrant expression of these receptors can contribute to tumor progression. NGF signaling can influence the expression of genes involved in cell growth, differentiation, and survival. Dysregulation of NGF signaling and associated epigenetic changes have been implicated in neurological and tumoral disorders. Epigenetic modifications, including DNA methylation and histone modifications, play a critical role in regulating gene expression and can contribute to tumor development and progression. The therapeutic potential of NGF and its receptors in tumors is being explored, with inhibitors targeting NGNerve Growth Factor (NGF) plays a dual role in inflammation and cancer, acting as both a pro-inflammatory and oncogenic factor, and as an anti-inflammatory and pro-apoptotic mediator depending on the context. This review summarizes the literature on NGF's role in regulating the inflammatory microenvironment and tumor cell growth, survival, and death. NGF is a neurotrophic factor involved in the growth, survival, and maintenance of neuronal and non-neuronal cells. It belongs to the family of neurotrophins, including BDNF, NT-3, and NT-4/5. NGF is synthesized as pro-NGF, which can have pro-apoptotic effects. NGF acts through two main receptors: TrkA and p75NTR. TrkA is a high-affinity receptor that activates signaling pathways involved in cell growth and survival, while p75NTR modulates NGF signaling and can influence cell death and survival. NGF can also interact with other receptors like sortilin and neuropilin-1, which are involved in cancer growth. Inflammation is a complex biological response that can contribute to tumor development and progression. Chronic inflammation can promote tumor initiation, growth, and metastasis by fostering angiogenesis, ECM remodeling, and immune suppression. NGF can influence inflammation by modulating immune responses and interacting with immune cells. NGF has been shown to support the survival and functionality of various immune cells, including mast cells, lymphocytes, macrophages, and natural killer cells. NGF can also promote the expansion of regulatory T cells, which can suppress the anti-tumor immune response. NGF plays a significant role in various aspects of cancer, including tumor growth, survival, and metastasis. It can promote tumor progression by stimulating cancer cell proliferation and suppressing apoptosis. NGF can also induce epithelial-mesenchymal transition (EMT), increasing cell mobility and invasiveness. NGF can influence the tumor microenvironment (TME) by modulating immune responses, angiogenesis, and the survival of cancer cells. NGF can also modulate the expression of cytokines and chemokines in the TME, influencing the function of immune cells and creating an immunosuppressive environment that favors tumor growth. NGF receptor expression in cancer varies, with Trk and p75NTR receptors playing significant roles in different types of cancer. Aberrant expression of these receptors can contribute to tumor progression. NGF signaling can influence the expression of genes involved in cell growth, differentiation, and survival. Dysregulation of NGF signaling and associated epigenetic changes have been implicated in neurological and tumoral disorders. Epigenetic modifications, including DNA methylation and histone modifications, play a critical role in regulating gene expression and can contribute to tumor development and progression. The therapeutic potential of NGF and its receptors in tumors is being explored, with inhibitors targeting NG