For cellular processes that are not directly related to pathogen resistance or defense, BIK1 does not utilize traditional defense-mediating hormones such as SA, JA, or ACC, but instead utilizes an herbicide, known as paraquat which produces ROIs. It is believed that SA, JA, and ACC have no effect on BIK1 induction because they are likely located downstream from the BIK1 gene, or it is possible that BIK1 operates completely independently. However, it is believed that BIK1 does play a vital role in the ET signaling pathway. Based on the signaling function of BIK1 in ET responses, it is believed that Botrytis-induced kinase1 accumulates response signals that it receives from upstream regulators and then integrates them into its own resistance mechanism.
BIK1 is a receptor-like cytoplasmic kinase (RLCK) that associates with a cell-surface receptor, FLS2, and a co-receptor kinase, BAK1 to transduce signals when a PAMP is detected. In order for BIK1 to be activated, site-specific phosphorylation must occur.