In the case of ROMK mutations in the Framingham study, ROMK R193P, H251Y, and T313FS caused hypertension resistance by ablating C-terminal glycosylation to ablate molecule trafficking, whereas P166S and R169H gain hypertension resistance through the abrogated PIP2 in the context of channel gating. The gene discussed is KCNJ1; the disease is hypertensive disorder.