This article describes a working hypothesis of the nature of the 'suicide condition' (SC). The authors contend that the SC emerges as a specialized result of two-phase impairment in the neuroimmunological 'inherited schematic representation' (ISR) involving: (a) the formation of a 'microcellular suicide' phenomenon; and (b) the establishment of a 'macro-organismic suicide' program. Our hypothesis, unlike earlier ones, is based on scientific evidence spanning diverse clinical diagnostic areas indicating that the SC is induced by a local histoincompatibility across distinct tissue structures and/or a remodeling of one or more neurimmunological ISR designs due to biophysical ion shunt bypass and neglect, whereas a normal neuroimmunological ISR complex produces an all-embracing organismic histocompatible tissue-syntonic-to-ego-syntonic expression. The presence of abnormal 'microcellular suicide' assemblies leads to cell syntonic-to-cell dystonic transformation and initiates the first modification phase by contaminating certain neurimmunological ISR programs which in turn trigger the onset of partial ego syntonic-to-ego-dystonic conversion. This is translated by the self-conscious experience as partial self-to-alien tissue translocation. These formations accumulate at a rate, arriving at the second phase in SC establishment when they reach a magnitude resolution that surpasses the organismic suicide threshold level and increase the amount of ego-syntonic-to-ego-dystonic inclusion. This is then translated by the self-conscious experience as a 'foreseeable and inescapable death' that is based on severe self-to-alien multiorgan substitution. The latter overcomes the rules and regulations prescribed by impulse-induced inner events, regardless of outer psychosocial events, and leads to an irrevocable drive to suicide.