In particular, Ca2+/calmodulin-dependent protein kinase 2 (CAMKK2), which is known to be overexpressed and overactive in DMD in relation to alteration in calcium homeostasis (Ye et al., 2016), can phosphorylate AMPK at the same site targeted by LKB1 (Tojkander et al., 2018) and might represent a likely pathway for basal AMPK phosphorylation (Fig. 8). Here, STK11 is linked to Duchenne muscular dystrophy.