NUAK1 and AMPK thus protect cancer cells from metabolic stress, which is a hallmark of most solid tumours.22, 23 This tumour-promoting activity of NUAK1 and AMPK is somewhat paradoxical, given that both are activated by LKB1, an established tumour suppressor: LKB1 phosphorylates AMPKα subunits on Thr172, and NUAK1 on Thr211, within the conserved T-loop of the kinase domain.1, 24 Notably, AMPKαT172 is phosphorylated by CamKK2 in response to calcium signalling,25, 26 suggesting that the T-loops of these kinases may be accessible to other upstream regulators in addition to LKB1. The gene discussed is CAMKK2; the disease is neoplasm.