Built upon the unified cellular G₀ and ΔGd theoretical system established in SFL-CELL-01 and SFL-CELL-02, this paper reconstructs the intrinsic mechanism of tumorigenesis under the Species Fixed Law framework. All somatic cells are born with a complete G₀ functional set, including a built-in proliferation limiting module that restricts excessive cell division and maintains stable tissue scale. Malignancy is not a case where cells evolve novel invasive capabilities; it arises from massive irreversible ΔGd(-) damage that completely breaks the proliferation control segment of the native G₀ architecture. Universal state equation shared across all SFL serials G = G₀ + ΔGd(+) − ΔGd(−) Minor physiological abrasion ΔGd(+) will not interfere with growth regulation and can be fully repaired by cellular metabolic systems. When persistent toxins, chronic inflammation and long-term tissue trauma accumulate excessive ΔGd(-), the proliferation suppression part of G₀ loses its original function. Without effective growth confinement, cells divide endlessly and form tumor masses, while invasion and metastasis are only derivative results of the collapsed regulatory framework rather than independent adaptive evolution. Traditional oncogenic mutation theories describe surface phenomena of structural damage, whereas this model locates the root cause in the breakdown of the inherent G₀ limiting module. Therapeutic strategies targeting tumor tissue only relieve superficial lesions; restoring the intact G₀ proliferation regulatory structure of precursor cells is the fundamental intervention direction. This cellular damage logic is consistent with the SLE pathological chain in SFL-CELL-02, forming a unified interpretation system for neoplastic diseases under the SFL framework, and can be further quantified via the lifespan mathematical model in the follow-up SFL-LS series.
FOO SENG ANG (Sat,) studied this question.