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An additional complicating factor is the fact that various components of the IGF1-Akt pathway exist as multiple isoforms, many of which are coexpressed in skeletal muscle (Table 1)

Herbst, R

Addressing the mechanism of the H 2 O 2 -induced macrophage death, immunoblotting for cleaved caspase-3, measurement of released IL-1 and IL-18, and use of nercostatin-1 did not support caspase-3-dependent apoptosis, inflammasome activation or necroptosis as the underlying cause of the cytotoxicity, respectively

(Okay, I do need to have at least a little fun with you.) With that out in the open, lets spend a few minutes demystifying this space