Here, we investigate the impact of cell size of cultured cells on rhythmicity; the role of influx signaling axes recruited by ACh, NE, AngII, CCK, BK, and insulin (Ins) acting via GPCR and RTK; receptors’ interplay at sub-threshold concentrations of hormones applied; the mechanisms of self-control based on the amplification of main PFL by other kinase-dependent loops; and the impact of obesity on the regulation of PLC-G and NOS-G. The gene discussed is INS; the disease is obesity disorder.