The pathophysiological mechanisms of the inflammatory response can be common to wound repair and tumor development. We propose that this response evolves in three phases, the nervous or immediate phase, the immune or intermediate phase, and the endocrine or late phase. In wound repair and in these phases, the interstitial space successively presents edema due to ischemia-revascularization and nutrition by diffusion (nervous phase), infiltration by leukocytes, which would mediate the nutrition of damaged neighbor cells (immune phase) and by angiogenesis, nutrition mediated by the capillaries that favor regeneration or scarring (endocrine phase). At the same time, in tumor development, it is considered that the cancerous cell successively occupies the interstitial space, expressing three different phenotypes: the hypoxia-reperfusion phenotype, with anaerobic glycolisis, oxidative stress and edema (dormant stage); the immune phenotype that expresses the functions corresponding to leukocytes, including the hyperproduction of pro-inflammatory mediators, lymphangiogenesis, the invasion of lymph nodes (N stage) and systemic inflammatory response syndrome; and lastly, the endocrine phenotype, in which the appearance of both local (tumor or T stage) and systemic (metastasis or M stage) angiogenesis induce a growing disease.