HIF1A and cancer: This gain in HIF-1 activation opens up two interpretations: a) as documented in a few cancer metabolism studies [33,34], HIF signalling can also be induced by various oxygen-independent mechanisms, collectively termed “pseudohypoxia”; thus, in trehalose-treated T98G cells, hypoxia-dependent ROS formation and pseudohypoxic mechanisms could act jointly; b) some negative regulators of HIF1-α could be depleted by the sustained autophagic process (as discussed later).