The association of the coding SLC30A8rs13266634 SNP with OS was due to a non-diabetogenic allele suggesting that, rather than modulating glucose homeostasis and insulin secretion [74], the effect attributed to the SLC30A8 locus on MM survival might be driven by a direct effect of Zinc in biological processes such as DNA and RNA stabilization [75], binding of protooncogenes to DNA [75–77] and the activation of IGF1 [26, 27, 61] or telomerase [78]. Here, IGF1 is linked to Miyoshi myopathy.