In summary, although consistent overexpression of KRASWT and KRASp.G12A/p.A146T/p.A146V proteins could only partially be achieved, our approach using two different stable transfection systems in two KRAS-wildtype MM cell line models still proved the capacity for activation of two major oncogenic pathways not only for the classical p.G12A mutant, but also for both p.A146 mutants. The gene discussed is KRAS; the disease is Miyoshi myopathy.