Taken together, the molecular mechanisms underlying the progression of CMT can be modeled as (i) the emergence of early oncogenic mutations (e.g., PIK3CA mutation) in benign tumors, (ii) subsequent acquisition of additional drivers accompanying malignant transformation (e.g., TP53 and KRAS mutations), and (iii) clonal domination of malignant subclones with genomic footprints (e.g., MAF and dN/dS ratios). This evidence concerns the gene PIK3CA and benign neoplasm.