Since the α-subunit is supposed to play a prominent role in the ENaC current activation by TNF and TIP peptide, we investigated whether TNF and solnatide can also enhance αβγ-ENaC current in α-ENaC loss-of-function frameshift mutants, i.e., αI68fs, αT169fs, αP197fs, αE272fs, αF435fs, αR438fs, αY447fs, αR448fs, αS452fs, and αT482fs (Table 2), which have been reported to cause PHA1B. This evidence concerns the gene A1BG and pseudohypoaldosteronism, type IB1, autosomal recessive.