The long-tail distribution of SM plays a major role in explaining the results showed in (Fig. 5): more than 80% of all registered SM configurations involve TP53 or PIK3CA or both (two of the most mutated genes in BC patients); on one hand we see the major role played by highly mutated genes in causing frail gene networks, on the other hand we register both a ρ variability within SM configurations involving highly mutated genes: the co-mutations with more rarely mutated (and most of the times marginal) genes characterizing frail SM configurations. This evidence concerns the gene PIK3CA and breast cancer.