The model introduced in this study (which focused on two very general cancer and immune biomarkers) can be easily generalised (see the discussion in [24]) to incorporate more complex aspects of ovarian cancer evolution: different cancer clone populations with different growth rates and different surface markers [51], or changes in the core molecules of different canonical pathways (such as PTEN, notch, PI3K/AKT, etc.)[51], or multiple cancer/immune biomarkers that might be associated also with different subtypes of ovarian carcinoma [52]. This evidence concerns the gene AKT1 and cancer.