This acquired resistance suggests the activation of adaptive and compensatory mechanisms, e.g. up-regulation of pro-angiogenic factors other than VEGF (targeted by bevacizumab), vascular co-option and vascular mimicry.15,16 The cancer stem cell population may also be involved in the secondary drug resistance and tumor relapse, as previously shown.29,30 Unfortunately, the degradation of the patient’s health condition was not anymore compatible with a new tumor sampling procedure and thus a follow-up PFP could not be envisaged. This evidence concerns the gene VEGFA and neoplasm.