WNK1 (With No Lysine(K) 1) is a ubiquitously expressed serine/threonine kinase containing several splice variants of clinical significance. These splice variants are known to have tissue-specific expression patterns. In particular, the large exon, called HSN2, is selectively expressed in neuronal tissues, and during development, and is named because mutations in the HSN2 exon are associated with hereditary sensory and autonomic neuropathy, type II (HSAN2). The HSN2-containing WNK1 transcripts are enriched in primary afferent dorsal root ganglion neurons, which are the sensory neurons that become damaged and dysfunctional during HSANII disease progression. This observation implies that expression of HSN2-containing WNK1 transcript variants in DRG neurons is required for survival and/or function of these neurons. Using long-read RNA-Sequencing we further refined the exon-level expression of WNK1 in human DRG. The expression of HSN2-containing WNK1 splice variants in DRG was similar to total WNK1 expression but was not uniform across all neurons. We hypothesized enrichment of HSN2-containing transcripts in nociceptive subpopulations, examining HSN2 expression in combination with nociceptive neuronal markers. However, overall, HSN2 was observed at lower levels in neurons encoding the precursor for Substance P peptide (TAC1). Conversely, HSN2 is enriched in large diameter human sensory neurons expressing the mechano-transducing ion channel gene PIEZO2. These results clarify the expression pattern of HSN2-containing WNK1 splice variants in human nociceptive tissues, and indicate that their expression, while ubiquitous, is enriched in proprioceptive large fibers. These data clarify the underlying molecular-cellular basis for HSANII neuropathology. The Intramural Research Program at the NIH Clinical Center.