Similar to what is observed in mouse models of ALS, M102 treatment also leads to increased expression of HSF1 in patient-derived iAstrocytes (Fig. 5F, G, unpaired t-test), indicating that M102 is a dual activator of the NRF2-ARE and HFS1-HSE pathways in vitro. The gene discussed is HSF1; the disease is amyotrophic lateral sclerosis.