Previous research in panNETs13 demonstrated that CIN is the result of the activation of the alternative lengthening of telomeres (ALT) pathway, a telomerase-independent mechanism of telomere maintenance, and multiple studies showed a robust correlation between tumor size, ALT activation, and loss of DAXX/ATRX, mainly as consequence of gene mutations13,14,17. This evidence concerns the gene GPT and neoplasm.