An shRNA-mediated KRAS-knockdown in this cell line, however, had no influence on MEK-/ERK-signaling while a KRAS knockdown in the KRASp.G12A mutant MM cell line MM1.S, which is neither affected by KRAS CN-gains nor increased mRNA expression, led to reduced ERK-activity and survival [10], coherent with the activation of the RAS/MAPK pathway in our current overexpression experiments of KRASp.G12A in HEK293, JJN3 and OPM2 cells. This evidence concerns the gene KRAS and Miyoshi myopathy.