Previouswork showed that nilotinib suppresses p38 phosphorylation in musclestem cells, impairing myogenic differentiation and altering ERK1/2and AKT signaling. More recently, itwas demonstrated that nilotinib mitigates LPS-induced neuroinflammationand memory impairment in wild-type mice by inhibiting p38 and STAT3phosphorylation in microglia and astrocytes, resulting in decreasedexpression of IL-1β, IL-6, and C7OX-2. These findings implicate p38 as a biologically relevant target ofnilotinib in both peripheral and CNS tissues. The gene discussed is AKT1; the disease is memory impairment.