NFKB1 and Hutchinson-Gilford progeria syndrome: Consistent with our analyses, previous studies showed that defects in the nuclear lamina, relevant to HGPS, are associated with the activation of the NF‐kB pathway, and that elevated CD36 expression promotes the activation of the NF‐kB pathway, leading to tissue damage and chronic inflammation (Han et al. 2021; Osorio et al. 2012).