OSU-03012: How can this direct PAK1 inhibitor activate the kinase AMPK?

So far all these anti-PAK1 products that activate the tumor suppressing
LKB1/AMPK kinase cascade are natural products （CAPE, curcumin, resveratrol,
capsaicin/capsiate, emodin, metformin and salidroside) and not ATP antagonists
that bind directly the ATP-binding pocket of the oncogenic kinase PAK1.
However, according to the 2007 paper from Mathew Ringel's group at OSU (Ohio
State University), the synthetic chemical compound 「OSU-03012」 is clearly
an ATP antagonist that binds the ATP-binding pocket of PAK1 and inactivate
this kinase. Interestingly, in 2010 Chang Fang Chiu's group at China
Medical University in Taiwan found that this ATP antagonist activates AMPK,
but only in the presence of “Gleevec” (ABL/c-Kit inhibitor)...

Well, in a common sense of enzymologists, it is very unlikely that
the ATP antagonist (competitive inhibitor!) activate this kinase by
its direct binding to the ATP-binding pocket of AMPK or its activator LKB1.
Thus, it is more likely that its inhibition of PAK1 indirectly leads to
the activation of the LKB1-AMPK cascade somehow. The most likely scenario
would be that PAK1 normally inactivates either LKB1 or AMPK, and OSU-03012
reactivates this kinase cascade by blocking PAK1. If this notion is proven
to be true, the "equation" (Un-PAKing=Activating LKB1/AMPK) for health and
longevity would be fully established in both directions:

LKB1 inactivates PAK1, and PAK1 inactivates LKB1/AMPK.

In this context, it would be of great interest to note that the tumor suppressor
"Merlin", an NF2 gene product, directly inactivates the oncogenic kinase
PAK1, whereas PAK1 phosphoryaltes "Merlin" at Ser 518 to inactivate its
tumor suppressor activity. Such a precedent makes us imagine (laterally
think!) that the tumor suppressor LKB1 inactivates PAK1, whereas PAK1 blocks
the tumor suppressive LKB1/AMPK kinase cascade.