In the current study, the effect of HSF1 over-expression in a mouse model of ALS was examined and found to significantly delay loss of bodyweight, disease onset, early disease, and survival in the 25th percentile suggesting that enhanced control of protein surface hydrophobicity by upregulating HSF1 is a potential target for the treatment of ALS and other proteinopathies. The gene discussed is HSF1; the disease is amyotrophic lateral sclerosis.