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Although the ectopic expression of genes that regulate differentiation has been observed in various cancers, its significance has not been fully investigated. In this article, based on the biochemical premise that “new biological responses do not fundamentally arise from mutations,” I redefine the role of ectopic expression in carcinogenesis and propose the “carcinogenic chimera cell (CCC) hypothesis.” The CCC hypothesis posits that ectopic expression of genes contributes to carcinogenesis via four mechanisms: (1) execution of their original functions, (2) expression of latent functions, (3) dysregulation of differentiation, and (4) inhibition of differentiation. This hypothesis provides a comprehensive explanation for the characteristics of cancer, including atypia, glycosylation defects, invasiveness, tissue-type diversity, and plasticity. Additionally, it complements and clarifies the molecular mechanisms of the traditional aberrant differentiation hypotheses and offers a perspective that integrates and encompasses existing theories such as the mutation theory, multistage carcinogenesis theory, epigenetic theory, cancer stem cell theory, and clonal evolution theory. Furthermore, this hypothesis introduces the concept of “non-mutational drivers,” a new type of cancer gene, expanding the definition of malignancy. This study provides a theoretical foundation for the development of molecular markers and new molecule-targeted drugs for diagnostic and therapeutic applications.