To determine whether this effect was attributed to the inhibition of CDKs and GSK‐3 by KEN,[24] we assessed ADAM10 protein level in cells treated with the KEN analog alsterpaullone (ALS) and AT7519 that has a different structure.[25] Surprisingly, whereas a slight but not significant increase of m‐ADAM10 protein levels was found in ALS‐treated cells (0.5 to 10 μM, Figure 1C), no significant alteration of m‐ADAM10 was detected in cells incubated with AT7519 (1 to 20 μM, Figure 1D), suggesting that enhancement of ADAM10 was dependent on the unique structure of KEN rather than kinase activity. The gene discussed is ADAM10; the disease is amyotrophic lateral sclerosis.