In hematological tumors such as T-ALL, AMPK has been shown to restrain tumor growth [13], and pharmacological activation of AMPK can slow leukemic cell growth through inhibition of mammalian target of rapamycin complex 1 (mTORC1) signaling [14], p38 MAPK [15], or unfolded protein response signaling [16]. This evidence concerns the gene PRKAA1 and neoplasm.