However, with the recently reported achievement of clinically relevant responses in some MM patients in a phase I Akt inhibitor trial [18] the possibility for future inclusion of PI3K/Akt inhibition in targeted MM therapies has drawn nearer, and comprehensive knowledge concerning the organisation and ramifications of PI3K-mediated oncogenic signalling in MM is therefore of critical importance for its successful clinical implementation. Here, PIK3CA is linked to Miyoshi myopathy.