This observation indicated that both ERK and AKT were downstream kinases to NGF-TrkA signaling in MM cells, although ERK showed a sustained basal state of endogenous phosphorylation, while in a dose–response assay (Additional file 2: Figure S4) AKT phosphorylation seemed to be more dependent on NGF-TrkA activation. This evidence concerns the gene AKT1 and Miyoshi myopathy.