Protein homeostasis, or proteostasis, refers to a proper balance between 
synthesis, maturation, and degradation of cellular proteins. A growing body of 
evidence suggests that the ribosome serves as a hub for co-translational 
folding, chaperone interaction, degradation, and stress response. Accordingly, 
in addition to the chaperone network and proteasome system, the ribosome has 
emerged as a major factor in protein homeostasis. Recent work revealed that high 
rates of elongation of translation negatively affect both the fidelity of 
translation and the co-translational folding of nascent polypeptides. 
Accordingly, by slowing down translation one can significantly improve protein 
folding. In this review, we discuss how to target translational processes to 
improve proteostasis and implications in treating protein misfolding diseases.