NFKB1 and androgen insensitivity syndrome: These results could be explained by that (a) lnc‐ITSN1‐2 suppressed several gene expression and inhibited their anti‐inflammatory effect (including miR‐107, miR‐125a, and miR‐146a [abovementioned]) to cause the activation of pro‐inflammatory pathways (including NF‐κB pathway and TRL pathway), thereby upregulating these pro‐inflammatory markers (including CRP, TNF‐α, IL‐1β, and IL‐6), which eventually promoted inflammatory response and increased diseases severity in AIS patients.