These include antitau antibodies and agents that stabilize microtubules, methods to increase the expression and release of progranulin, modulating autoimmunity and neuroinflammation (particularly applicable for GRN mutations), as well as using antisense oligonucleotides to silence toxic C9orf72 messenger RNA messengers—strategies which hold promise in targeting the root mechanisms while making advancements in FTD treatment [8]. The gene discussed is GRN; the disease is frontotemporal dementia.