Vermani 3 oxidative cell stress activates the MAPK signaling pathway, causing an inflammatory response. In these brain diseases, cellular stress is caused by misfolded amyloid-beta and tau proteins, while in BAG3 P209L MFM, cellular stress results from a lack of functional selective autophagy. Targeted activation of p38 in vivo has been shown to induce heart failure and a similar cardiac hypertrophy as that seen in the mutant mice, and the mutant mice also show increases in inflammatory infiltrates and activation of NF-κB, a prototypical proinflammatory signaling pathway, which is characteristic of p38 activation. All these evidence points to targeted inhibition of p38 as an effective treatment of BAG3 mutation caused MFM. Our research is the first attempt we know of to discover p38 inhibitors as a treatment for a genetic myopathy.