AKT1 and Miyoshi myopathy: Given the high genetic heterogeneity of MM [8,10,52] and the potential of IGF1R for oncogenic activity through the formation of hybrid receptors as well as through activating mutations, we chose HMCLs that represent different molecular aspects with relevance to IGF1R signaling, such as intrinsic AKT activity, AKT dependence [16,53] and the mutation pattern [10].