Most common AIP alterations result in amino acid substitutions or a truncated AIP protein particularly within the C-terminal, which contains three tetratricopeptide repeats (TPR) responsible for protein–protein interactions [3, 7] Such tumors containing AIP mutations typically have a tendency to occur in individuals at a younger age, to become larger and more aggressive [1–6], and to be resistant to somatostatin analogs which are the first-line drug therapy for acromegaly [3, 4, 8, 9]. The gene discussed is AIP; the disease is acromegaly.