Because BRAF KE expression in αCaMKII+ excitatory neurons or vGAT+ inhibitory neurons did not impair hippocampal-dependent learning and memory, we hypothesized that other cell types (i.e., nonneuronal cells) might be responsible for the mutant BRAF-associated deficits in learning and memory observed in RASopathy patients. Here, SLC32A1 is linked to RASopathy.