The expression of the sole alpha-subunit of muscle or brain sodium channels in frog oocytes mediates currents with a bimodal inactivation with an abnormal slow mode that is strongly depressed only by co-expression of the beta1-subunit. In contrast, in the expression of the alpha-subunit in the human embryonic kidney cell line, HEK-293, the slow mode is almost absent, suggesting an endogenous expression of the beta1-subunit. We have tested this hypothesis by reverse transcriptase-polymerase chain reaction. We found an abundant expression of mRNA encoding the beta1A splicing of the putative regulatory sodium channel subunit but no mRNA encoding the beta1-subunit in HEK cells. This finding is consistent with the idea that the endogenous beta1A-subunit is sufficient for suppressing the slowly inactivating mode of sodium currents by co-assembly with alpha-subunits, and calls attention to the reliability of effects attributed in HEK cells to alpha-beta1 co-expression.