Abstract: Clonality appears an essential pathogenesis for genetic instability and for aberrant cell/cell interactive adhesion contact phenomena towards creation of a neoplasm via several potential pathways of highly varied nature, including DNA strand duplication promoting mismatch repair. Indeed, a series of neoplastic type lesions ranging from breast carcinoma to thyroid, colorectal and asbestos-related neoplasms might constitute a highly varied multiplicity of pathways in carcinogenesis. Genetic instability appears centrally implicated as one paramount mechanistic pathway of progressiveness in neoplastic development and subsequent course. This would promote a highly varied mode of possible pathogenesis towards an infiltrative spread of autonomously or excessively proliferating cells. In terms of cell/cell contact promoting increasing dysplasia as seen in colorectal polyps and of inflammatory conditioning and cytokine contributory roles towards neoplasms as evidenced in asbestos related mesotheliomas, there would arise cell proliferation that both constitutes the creation of multisystem effects and also proves a strong inducer of further evolving carcinogenesis.One basic attribute of carcinogenic pathways is the initial creation of multiple promoting events that would be based on a core phenomenon of genetic instability. In overall yet specific terms, such an apparently great multiplicity in creation of carcinogenic events towards genetic instability would further induce evolving neoplasia. Such a phenomenon would depend on intercellular events biophysically determining the responsiveness of cells exposed to such highly varied potential carcinogenesis. Indeed, a strong reference point in carcinogenesis would relate specifically to the responsiveness of affected cells irrespective of actual carcinogenic agents of exposure and of action. Exposed cell responsiveness would evolve as genetic instability and altered cell/cell interactions promoting multiple injuries as inflammatory and reparative phenomena in such cellular aberrant responsiveness, this being generally of both hereditary and acquired origin.