Failed activation of the immune response to neoplastic cell proliferation and spread would implicate systems of exposure and of presentation of antigenic epitopes on cells. Such failure in antigenicity of tissue components would characterize primary inception of the lesion as a neoplasm that subsequently increases in size and progresses. It is with reference to inflammation as a mechanism of exposure and of presentation of antigen that one might envisage neoplastic and ischemic tissues as a dual coupling potentially related to both immune stimulation and activation of clones of lymphocytes, inflammatory cells and macrophages. Such cell components of tissue would participate in the realization of various compounding pathways of propagation involving cytokines and chemokines in inducing further progression of the neoplasm or in suppressing tumor growth and spread. Ischemia and post-ischemic perfusion injury of tissues appear applicable in inducing a coupled inflammatory and immune reactivity in various tissues including neoplasms.