This phenomenon is probably underpinned by a wide transcriptional rearrangement in these cell clones that allows for a rapid switch towards the PI3K/AKT pathway only when EGFR/MAPK pathway is fully suppressed, as a consequence of prolonged MAPK suppression and c-myc persistent deregulation, as suggested in another publication on breast cancer [27]. The gene discussed is AKT1; the disease is breast carcinoma.