This phenotypic switch was mediated through a non‐canonical interaction between Bmal1 and non‐muscle myosin heavy chain IIA (Myh9), which activated the MRTF‐SRF signaling pathway and increased AP‐1 transcriptional activity.[361] Nevertheless, BMAL1 has been revealed as a clinically relevant prognostic factor and biomarker for T‐cell‐based immunotherapies for melanoma patients,[362] suggesting a complex role of circadian genes in tumor immunity and progression. The gene discussed is BMAL1; the disease is melanoma.