To determine whether C98 was able to inhibit PI3K activity, a MM cell line OPM2 which displays high PI3K activity due to lack of PTEN, a negative modulator of the PI3K signaling pathway [16], was starved overnight followed by C98 treatment and subsequent stimulation with IGF-1, a critical trigger of PI3K signaling and a key growth factor in MM cell proliferation. The gene discussed is IGF1; the disease is Miyoshi myopathy.