Antarctic notothenioid fishes are noteworthy for their history of isolation and indications they lack the heat shock response. The mechanistic basis for stenothermy has not been fully elucidated, and some aspects of stenothermy could arise post-transcriptionally. Antarctic emerald rockcod (Trematomus bernacchii) were sampled after exposure to chronic and/or acute high temperatures, followed by assessment of proteomic responses in brain, gill, and kidney using tissue-specific DIA assay libraries. Few cellular stress response proteins were induced, and overall responses were modest in terms of numbers of differentially expressed proteins and their fold changes. Inconsistencies in protein induction across treatments and tissues are suggestive of dysregulation, rather than an adaptive response. Changes in regulation of translation in Antarctic notothenioids could explain these patterns. Some components of the “integrative stress response” that regulates translation are highly conserved (e.g., Ser-52 of eIF2α), but the eIF2α kinases GCN2 and PERK may have evolved along different trajectories in Antarctic fishes. Together, these observations suggest a novel hypothesis for stenothermy and the absence of a coordinated cellular stress response in Antarctic fishes.