<p><i>SCN2A</i> encodes the voltage-gated sodium channel Na_V1.2, a central regulator of action potential initiation and propagation in glutamatergic neurons, and one of the strongest single-gene risk factors for autism spectrum disorder. Premature termination codons in <i>SCN2A</i> are widely considered to produce uniform haploinsufficiency through nonsense-mediated mRNA decay, an assumption that underpins current mechanistic and therapeutic models. We generated two mouse lines carrying patient-derived mutations – <i>Scn2a</i>^{<i>Y84X/+</i>} (p.Tyr84UAA; early coding sequence) and <i>Scn2a</i>^{<i>R1627X/+</i>} (p.Arg1627UGA; terminal coding exon). We assessed allele-specific mRNA expression, Na_V1.2 protein expression, ex vivo whole-cell recordings, and behavioral phenotypes in these mice. Allele-specific RNA handling diverged by position: mRNA carrying Y84X engaged partial nonsense-mediated decay, whereas R1627X transcripts were at allelic balance. Despite this difference in RNA fate, Na_V1.2 protein was comparably reduced in both lines. Both variants slowed the action potential upstroke, with a larger decrement in <i>Scn2a</i>^{<i>Y84X/+</i>}. Spike threshold was depolarized only in <i>Scn2a</i>^{<i>Y84X/+</i>}. Mutant neurons showed reduced firing near rheobase. Both lines exhibited increased grooming, but <i>Scn2a</i>^{<i>Y84X/+</i>} alone showed greater exploration and a male-predominant rotarod learning deficit. Locomotion, sociability, and sensorimotor gating were preserved. In maximal electroshock testing, mortality was reduced in both lines without changes in seizure threshold or severity. Our results show that <i>SCN2A</i> premature termination codon position determines allele-specific effects on neuronal excitability and behavior, where both NMD and phenotypes of the <i>Scn2a</i>^{<i>Y84X/+</i>} line are more penetrant. These data challenge the assumption of uniform haploinsufficiency and directly support allele-tailored mechanistic studies and therapeutic strategies.</p>