IGF2 and bacterial infectious disease: We looked for specific conditions that could predispose siNET development and found no evidence of bacterial infections, the genotoxin colibactin, telomere lengthening or loss of imprinting of IGF2. In three patients with multi-focal tumors, we found germline mutations in the FANC DNA repair pathway, strongly linked to HR DNA repair34,35, which could explain the high number of chromosomal alterations observed in siNETs.