These two scenarios are not antagonistic, but can co-exist, as in the case of multiple myeloma (MM): growing in an hypoxic niche in bone marrow, MM has a canonical activation of HIF-1α that induces chemoresistance, but also the concurrent activation of oncogenic pathways (e.g. Wnt, Notch, Ras/MAPK-, PI3K, Akt/mTOR-, NF-kB-dependent pathways) that prevent the apoptosis induced by chemotherapeutic drugs [90, 105]. The gene discussed is AKT1; the disease is Miyoshi myopathy.