The M1 activation of the A2→A1 transition can be inhibited with both anti-TNFα medications (normally used for the treatment of inflammatory bowel disease and that has preliminary evidence for its neuroprotection in PD) [71] and glucagon-like peptide-1 receptor (GLP1R) agonists (used to control type 2 diabetes mellitus) [72]. This evidence concerns the gene GLP1R and type 2 diabetes mellitus.